Thursday, August 04, 2016

This anti-science creationist could be Vice-President of the United States of America

Thanks to PZ Myers for digging up this speech by Mike Pence in the House of Representatives [Mike Pence, creationist]. I think Pence is trying to make America great again by returning the country to the stone age.




275 comments :

  1. This anti-science creationist could be Vice-President of the United States of America

    There could be worst candidate for Vice-President of US. There could be someone who believes that life originated by accident but he can't provide one piece of evidence that swayed him to believe it.

    There could be someone who believes that live evolved from prokaryotic to eukaryotic even though there is not one piece of experimental evidence to support it and there are many missing pieces of the puzzle to this notion.

    There could be someone who believes that evolution happened even though on the molecular level evolution has been proven impossible as proven by experiments by Doug Axe and Ane Gauger ( who are considered by many creationists). They proved that evolution could not evolved new protein function in the time available. All one who disagrees can do is prove them wrong by performing the actual experiments rather than just criticizing others who do experiments.

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    1. Vote for Trump and Pence. If enough people agree with you America will get what it deserves.

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    2. Another creationist infestation. Cruglers blathers: There could be someone who believes that live evolved from prokaryotic to eukaryotic even though there is not one piece of experimental evidence to support it

      "Not one piece of experimental evidence" says creationist genius. I'm sure he searched PubMed for terms "evidence" "experiment" and "endosymbiotic theory" and showed there was no evidence.

      Ha ha, I'm kidding. Creationists don't know what PubMed is. They learn all their science from Ken Ham.

      He could have spent 10 seconds looking at Wikipedia:

      "Evidence that mitochondria and plastids arose from bacteria is as follows:[31][32][33]

      New mitochondria and plastids are formed only through a process similar to binary fission. Binary fission is the form of cell division used by bacteria and archaea.[citation needed]

      ...

      Transport proteins called porins are found in the outer membranes of mitochondria and chloroplasts and are also found in bacterial cell membranes.[35][36][37]

      A membrane lipid cardiolipin is exclusively found in the inner mitochondrial membrane and bacterial cell membranes.[38]

      Some mitochondria and some plastids contain single circular DNA molecules that are similar to the DNA of bacteria both in size and structure.[39]

      Genome comparisons suggest a close relationship between mitochondria and Rickettsial bacteria.[40]

      Genome comparisons suggest a close relationship between plastids and cyanobacteria.[41]

      Both mitochondria and plastids have small genomes compared to bacteria and neither organelle would be capable of surviving outside the cells where they are found. This is consistent with an increased dependence on the host after forming an endosymbiosis.[citation needed]

      Many genes in the genomes of mitochondria and chloroplasts have been lost or transferred to the nucleus of the host cell. Consequently, the chromosomes of many eukaryotes contain genes that originated from the genomes of mitochondria and plastids.[39]

      Mitochondrial and plastid ribosomes are more similar those found in bacteria (70S) than those found in eukaryotes.

      Proteins created by mitochondria and chloroplasts use N-formylmethionine as the initiating amino acid, as do proteins created by bacteria but not proteins created by eukaryotic nuclear genes or archaea.[42][43]

      Much of the internal structure and biochemistry of plastids (e.g. the presence of thylakoids and particular chlorophylls) is very similar to that of cyanobacteria.[citation needed]
      ...

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    3. Continuing:

      "Secondary endosymbiosis occurs when the product of primary endosymbiosis is itself engulfed and retained by another free living eukaryote. Secondary endosymbiosis has occurred several times and has given rise to extremely diverse groups of algae and other eukaryotes. Some organisms can take opportunistic advantage of a similar process, where they engulf an alga and use the products of its photosynthesis, but once the prey item dies (or is lost) the host returns to a free living state. Obligate secondary endosymbionts become dependent on their organelles and are unable to survive in their absence...

      One possible secondary endosymbiosis in process has been observed by Okamoto & Inouye (2005). The heterotrophic protist Hatena behaves like a predator until it ingests a green alga, which loses its flagella and cytoskeleton, while Hatena, now a host, switches to photosynthetic nutrition, gains the ability to move towards light and loses its feeding apparatus.[45]

      The process of secondary endosymbiosis left its evolutionary signature within the unique topography of plastid membranes. Secondary plastids are surrounded by three (in euglenophytes and some dinoflagellates) or four membranes (in haptophytes, heterokonts, cryptophytes, and chlorarachniophytes). The two additional membranes are thought to correspond to the plasma membrane of the engulfed alga and the phagosomal membrane of the host cell...

      Despite the diversity of organisms containing plastids, the morphology, biochemistry, genomic organisation, and molecular phylogeny of plastid RNAs and proteins suggest a single origin of all extant plastids – although this theory is still debated."

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    4. So, Cruglers clearly is blathering when he says "not one pice of evidence." But we need some more comedy, so there's this:

      "There could be someone who believes that evolution happened even though on the molecular level evolution has been proven impossible as proven by experiments by Doug Axe and Ane Gauger ( who are considered by many creationists)."

      Herpy derp, Cruglers doesn't know that

      Problem 1. Axe and Gauger only try to mutate one modern protein into its modern "cousin" protein. They don't work backward to the common ancestor. This is like disproving the hypothesis "My cousin and I have a common grandfather" by doing surgery to turn me into my cousin. When you can't turn something directly by a straight path into its cousin, this is NOT a test of the hypothesis of common descent. You have to work backward from one species to the imputed common ancestor, then forward from the common ancestor to the other modern species.

      The protocol for doing this the right way was described in detail by Joe Thornton's lab and is called Ancestral Sequence Reconstruction (ASR) but Axe and Gauger won't use it because it doesn't give the answer they decided on.

      Here's a short list of papers on Ancestral Sequence Reconstruction.

      There are a lot of papers using the ASR method but none are by Axe and Gauger. The method has medical uses because ASR has allowed Thornton's lab to deduce previously unknown functions for currently existing enzymes.

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    5. Problem 2. Doug Axe is frequently cited for a bullshit probability calculation saying that only 1 out of 10^77 possible sequences of amino acids will make a functional protein. The problem is his terrible math, not evolutionary theory.

      For one thing, he did one experiment that only searched for ONE possible biological function (ATP binding) out of all possible biological functions. Of course proteins could flip functions during the course of evolution.

      Second, he started his experiment with a mutant protein that was already partially disabled, then sampled only a few mutations around it. So he's already NOT starting from the wild type protein.

      If the wild type protein were in a "hill" of function space connected by a "high ridge" of functional sequences to a different "hill" with a different function, Axe's experiment wouldn't detect this, because he started with a mutant that was part of the way down the "hill" into the ocean beneath, and explored the landscape off the shore.

      More detail on math errors in Doug Axe's 2004 paper on "1 in 10^77 probability" at Panda's Thumb.

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    6. Diogenes,

      I applaud your perseverance and stamina. Ideologues like Cruglers incessantly return to present arguments that were debunked decades ago as if they were brand new. Creationists don't have anything new that they didn't have since before I was born. They just keep smearing lipstick on that pig and dragging it out to obfuscate.

      It's the antithesis of science: creationists try to confuse, rather than clarify the situation. That is the only point of Axe & Gauger. If they wanted to provide evidence for ID, they would come up with a theoretical framework that makes predictions that distinguish it from modern evolutionary theory. Instead, they create straw men, knock them down and declare victory.

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    7. Cruglers, your earlier post about your textbooks providing no evidence for evolution indicates you had a lousy science education. However, you don't need to be stuck in ignorance. As Diogenes has shown, there's a lot of evidence about the issues you've brought up. Read something that provides the evidence. Again, I'd recommend "Why Evolution Is True," but there are other books.

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    8. Diogenes,

      Unfortunately, you have NOT provided 1 (one piece of evidence) of experimental evidence for your claims.

      The next step in your claims is to provide FURTHER real-deal-experimental-evidence for your claims.

      Then, the next step would be to do some further real science but you seem to be immune to that... I wonder why?

      Don't forget to attach some links to the science you and other determined atheists have done!

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    9. Cruglers, your response has two basic errors.

      First, science is based on OBSERVATIONS. The purpose of experiments is to allow clearer, more detailed, more exact observations. Therefore, Diogenes' list of observations that are evidence for the relationship between mitochondria, chloroplasts, and bacteria are exactly the kind of evidence you would be looking for if you knew what you are trying to pretend you're doing.

      Second, that link to ancestral sequence reconstruction provides experimental evidence about how genes/proteins evolve. So saying you weren't given experimental evidence is incorrect.

      You don't know what science is about. You don't follow up on the evidence you've asked for when it's given to you. I had hoped you were merely ignorant about evolution, but sadly that's not the case.

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    10. Vote for Trump and Pence. If enough people agree with you America will get what it deserves.

      Larry, We both know that no matter who inherits the "white-dome", the majority of the population of US will not be affected by "so-called-change". On average, there will be anywhere from 45-47 million of american citizens on food stamps. Do you know what food-stamps are called among the rich? "Eat for free and shut up you poor morons and be glad!"

      This is not joke. US is considered to be the riches nation in the world with a quarter of their citizens not being able to make it to the 1st of the month. Who is behind this propaganda that US is the greatest country in the world?Wanna take a guess?

      Why would I vote for any government that will not change this reality? Give me one sound reason, and I will consider your side of the story seriously.

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    11. Do you know what food-stamps are called among the rich? "Eat for free and shut up you poor morons and be glad!"

      Well that's them rich people for you... they have the luxury of obsuscating with 12 words when they could have been transparent with 2.

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    12. Cruglers, the United States no longer has "food stamps" - you may know that, you may not, it's not possible for me to gauge whether you are simply using an old term due to lack of information or for some other reason.

      If your response was in any way meant to imply that the SNAP program provides a free path to high on the hog eating for the people who receive it, I'll conclude that your terms were used for the "some other reason" option.

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    13. Crugler appears quite unfamiliar with the American political system. There is no "white dome" on the White House where the president lives. The white dome is on the Capitol building where Congress meets. Pence is running for Vice President who lives in a different building.

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    14. Cruglers attempts a mere denial strategy-- he originally falsely stated there is no evidence for endosymbiosis, "there is not one piece of experimental evidence to support it", so I listed a bunch of evidence including experimental evideence, then Cruglers flatly denies that experimental evidence is experimental evidence: "Unfortunately, you have NOT provided 1 (one piece of evidence) of experimental evidence for your claims." In fact I listed several.

      In the face of evidence, Cruglers simply cries "There is no evidence!" without detail or explanation. Anyone can do that to any kind of scientific evidence. Round Earth, anything.

      It's incumbent on Cruglers to go through my list and explain what's wrong with each bit of evidence-- or at least, pick the best 3 lines of evidence and refute those.

      Cruglers will not even pick one line of evidence and explain what's wrong with it, or show that he even understands it. So I will choose one line of evidence that I already cited.

      Tell us how this evidence for endosymbiosis is not experimental? Do not simply reply with "Nuh-UH!"

      From Wikipedia:

      "Secondary endosymbiosis occurs when the product of primary endosymbiosis is itself engulfed and retained by another free living eukaryote... Some organisms can take opportunistic advantage of a similar process, where they engulf an alga and use the products of its photosynthesis, but once the prey item dies (or is lost) the host returns to a free living state. Obligate secondary endosymbionts become dependent on their organelles and are unable to survive in their absence...

      One possible secondary endosymbiosis in process has been observed by Okamoto & Inouye (2005). The heterotrophic protist Hatena behaves like a predator until it ingests a green alga, which loses its flagella and cytoskeleton, while Hatena, now a host, switches to photosynthetic nutrition, gains the ability to move towards light and loses its feeding apparatus.[45]

      The process of secondary endosymbiosis left its evolutionary signature within the unique topography of plastid membranes. Secondary plastids are surrounded by three (in euglenophytes and some dinoflagellates) or four membranes (in haptophytes, heterokonts, cryptophytes, and chlorarachniophytes). The two additional membranes are thought to correspond to the plasma membrane of the engulfed alga and the phagosomal membrane of the host cell..."


      Why are observations of phagosomes in Hatena engulfing green alga and forming an endosymbiotic relationship with them not evidence for endosymbiosis?

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    15. Furthermore, Crugler completely ignored my refutation of his absurd claim "on the molecular level evolution has been proven impossible as proven by experiments by Doug Axe and Ane Gauger ( who are considered by many creationists)." Crugler never explained HOW or IN WHAT WAY Axe and Gauger had proved evolution at the molecular level to be "impossible."

      As I pointed out, there meager experiments are irrelevant to testing evolutionary hypotheses and are technologically way behind the times. I could have listed many more lines of evidence.

      Here's yet another line of evidence. Recall that Axe and Gauger claimed that the odds of a random string of functional proteins having a biological function is only 1 in 10^77.

      But here is an experiment from the lab of Nobel Prize winner Jack Szostak, based on testing a library of totally randomized strings of amino acids found one functional protein out of 10^12 random strings.

      “Functional proteins from a random-sequence library.” Anthony D. Keefe & Jack W. Szostak. Nature, v. 410 (6829). 5 April 2001. p 715-8. Abstract: Functional primordial proteins presumably originated from random sequences, but it is not known how frequently functional, or even folded, proteins occur in collections of random sequences. Here we have used in vitro selection of messenger RNA displayed proteins, in which each protein is covalently linked through its carboxy terminus to the 3’ end of its encoding mRNA1, to sample a large number of distinct random sequences. Starting from a library of 6 x10^12 proteins each containing 80 contiguous random amino acids, we selected functional proteins by enriching for those that bind to ATP. This selection yielded four new ATP- binding proteins that appear to be unrelated to each other or to anything found in the current databases of biological proteins. The frequency of occurrence of functional proteins in random-sequence libraries appears to be similar to that observed for equivalent RNA libraries.

      They tested 6 * 10^12 randomized strings of 80 amino acids each and four bound ATP, so that's approximately one functional string every 10^12 random sequences. If true, then Axe and Gauger's result is off by a factor 10^65 which is 10^77/10^12.

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    16. Diogenes

      "As I pointed out, there meager experiments are irrelevant to testing evolutionary hypotheses and are technologically way behind the times. I could have listed many more lines of evidence.

      Here's yet another line of evidence. Recall that Axe and Gauger claimed that the odds of a random string of functional proteins having a biological function is only 1 in 10^77.

      But here is an experiment from the lab of Nobel Prize winner Jack Szostak, based on testing a library of totally randomized strings of amino acids found one functional protein out of 10^12 random strings."

      Why do you think these experiments are getting such different results?

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    17. Very, very simple: Axe and Gauger insist on using incorrect probability math, and formulating experiments to "prove" the wrong thing in service to that math.

      Axe and Gauger have shown, in effect, that the chance of *a particular protein* winning their "lottery" is 1 in 10^77. This is the wrong experiment if you want to find the answer to the correct question, the one Szostak, asked and formulated his experiment to answer: What are the chances of *any* protein winning the evolutionary "lottery"? This result is far more likely.

      This is exactly the same math that correctly tells you there is a miniscule chance *you* will win the PowerBall - about 175 million to 1. At about 100 drawings every year, *you* might expect a win about once every 1.75 million years. But *someone* wins the PowerBall every few weeks.

      Every time you read about someone winning the PowerBall, remember it's confirmation Axe and Gauger are wrong.

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    18. Lee Witt,

      "SNAP participation in May 2014 dropped by 22,294 to 46,225,054 people; that represented a decrease of 1,410,172 people compared with May 2013. This is the sixth consecutive month that SNAP participation has averaged below 47 million people."

      http://frac.org/reports-and-resources/snapfood-stamp-monthly-participation-data/

      Who cares what the program is called now? The number is still pretty much the same-47 million Americans need to receive food assistance in the richest country in the world.
      Do you believe this number is going to drop to 40 million if I pro-evolution government is in the white-house instead of pro-creationism?


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    19. Judmarc
      "This is exactly the same math that correctly tells you there is a miniscule chance *you* will win the PowerBall - about 175 million to 1. At about 100 drawings every year, *you* might expect a win about once every 1.75 million years. But *someone* wins the PowerBall every few week"

      How many people would win the lottery if there were 20 balls instead of 6? How many proteins have less than 10 amino acids?

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    20. Bill -

      Is 1 in 10^12 too high a number for you? Why are you changing the subject? On the topic of amino acids and functional proteins, Szostak and Axe and Gauger were working with the same number of amino acids or "balls." The difference is not in that number, but in the fact that Axe and Gauger were calculating probabilities of obtaining *one particular* functional protein, while Szostak was calculating probabilities of obtaining *any* functional protein. This is precisely the mathematical difference between the chance of *you* (or any other specific person) winning the lottery and the chance of *anyone* winning the lottery.

      Sorry, Bill, won't let you sidetrack this one under the guise of just asking questions.

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    21. "SNAP participation in ..." (just to set the target for this post)

      My question was the reason you used that term. Reagan began using it with a nasty racist overtone, and a good sized group of people doing so. My question was whether you were among them - you haven't answered.

      I certainly believe the number in the program has a better chance of decreasing if the government is under Democratic control (I don't know whether Hillary understands science and evolution or not, but since she is well educated there is a good chance she does) than it would under the control of Donald Trump (I don't know which side he comes down on either, but given his ramblings about vaccines it's probably a fair bet he'd come down on the side of ignorance and pick creationism - certainly if he thought that would garner more votes than he would get by saying "I side with science"). Remember, it was the policies of a science denying man that contributed mightily to destroy the economy in the early 2000s.

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    22. Judmarc
      "The difference is not in that number, but in the fact that Axe and Gauger were calculating probabilities of obtaining *one particular* functional protein, while Szostak was calculating probabilities of obtaining *any* functional protein. This is precisely the mathematical difference between the chance of *you* (or any other specific person) winning the lottery and the chance of *anyone* winning the lottery."

      You don't have the analogy right and thats why I am asking you the questions. Your lottery example is flawed and I thought I had shown you this in the past.

      The lottery example only works in small populations of sequences. Once the number of balls goes up even with the population of our planet your chance of winning is very remote.

      Both the Axe paper and the Szostak paper involve binding to a specific molecule.TEM-1 penicillinase is the molecule in the Axe experiment and ATP is the molecule in the Szostak experiment. That is not the reason for the probability difference.

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    23. I'm not sure where Axe and Gauger made their error, but note that their method necessarily requires mathematical extrapolation, while Szostak's method doesn't. Szostak and co-workers actually created a library of 6 *10^12 random proteins with 80 amino acids and counted how many bound ATP.

      By contrast, Axe and Gauger certainly did not create a random library of 10^77 proteins because no one could create that much in a lab. Their method involved starting with a mutant sequence that was slightly disabled relative to the wild-type, off the peak of a fitness hill. Then they did some random mutants in its vicinity. Certainly not 10^77. They counted up the mutants that retained the original protein's function (not checking for new functions) and then did some calculations to extrapolate out to 10^77. I forget the mathematical details of how they got it. Szostak's experiment is more direct counting, Axe's uses a bunch of assumptions.

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    24. Hi Diogenes -

      I'm not sure where Axe and Gauger made their error.... They counted up the mutants that retained the original protein's function (not checking for new functions)

      There's the error I was talking about, and the answer to Bill Cole. They looked for *only one specific "winner"* (proteins retaining the specific *identical* function to the original one) and *not* proteins with *any* function. Right there is the basic reason for the difference, which, I repeat, is the same thing that makes the difference between you or I having a 175 million to 1 chance of winning the lottery and the fact that *someone* wins the lottery every few weeks.

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    25. Once the number of balls goes up

      I certainly agree, Bill, that your explanation is balls.

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    26. @Bill Cole

      You don't have the analogy right and thats why I am asking you the questions. Your lottery example is flawed and I thought I had shown you this in the past.

      The lottery example only works in small populations of sequences. Once the number of balls goes up even with the population of our planet your chance of winning is very remote.


      That's not necessarily so. You can't determine the odds of someone winning just by knowing the numbers of balls that are used to determine the winning number. You also need to know how many people hold tickets with potential winning numbers. That's the part that Axe and Gauger did not calculate.

      But this has already been explained to you, many times. For some reason, you continue not to comprehend this simple idea. I wonder why that is.

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    27. lutesuite
      "That's not necessarily so. You can't determine the odds of someone winning just by knowing the numbers of balls that are used to determine the winning number. You also need to know how many people hold tickets with potential winning numbers. That's the part that Axe and Gauger did not calculate. "

      First, Axe did calculate multiple solutions or the odds would have been 1/20^150 based on the probability calculation.

      Second human populations are not relevant once the number of lottery balls gets above a certain number. You and Judmarc are not grasping this concept yet. The math is the population divided by the probability. If the probability is 1/!0^50 and the population is 10^10(larger than earths population) the probability of a winner is 1/10^40.
      The number of needles in the haystack is irrelevant if the haystack is big enough.



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    28. Diogenes
      "By contrast, Axe and Gauger certainly did not create a random library of 10^77 proteins because no one could create that much in a lab. Their method involved starting with a mutant sequence that was slightly disabled relative to the wild-type, off the peak of a fitness hill. Then they did some random mutants in its vicinity. Certainly not 10^77. They counted up the mutants that retained the original protein's function (not checking for new functions) and then did some calculations to extrapolate out to 10^77. I forget the mathematical details of how they got it. Szostak's experiment is more direct counting, Axe's uses a bunch of assumptions."

      This is pretty accurate. Axe did extrapolate the probability in two steps first for folds (10^33) that had the profile to perform the function then if the e coli could grow in an environment with penicillin. (10^64) he then paired the calculation to (10^77) combining the two(10^97) and a reduction for some reason.

      The weakness of this experiment is the probability estimation as you pointed out the strength is the use of survival (e coli able to multiply in a hostile environment) as a direct measurement of enzyme effectiveness vs simple an assay of reaction frequency.

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    29. I have to re-read Axe's paper.

      There are more papers nowadays on how many sequences will form stable folds, and on proteins that are functional while unfolded. Folding is not strictly necessary, but typical of the proteins that can be easily studied in the lab.

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    30. Note, and perhaps this is important, that Szostak's random library method does not, to my knowledge, require the proteins to be folded.

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    31. @ Bill Cole

      First, Axe did calculate multiple solutions or the odds would have been 1/20^150 based on the probability calculation.

      Oh, I'm sure he did some random calculations to come up with some bullshit number. But, if you think his number has any relevance to real world situation, kindly explain the rationale here.

      Second human populations are not relevant once the number of lottery balls gets above a certain number.

      No, human population remains completely irrelevant. You need to know the number of potential winning tickets that are being held. What if they were giving tickets away for free, and everyone on earth decided to get a billion tickets each. Wouldn't that affect your calculation of the odds of someone winning?

      This concept is so childishly simple, that I can't help feeling that your failure to understand or accept it is willful.

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    32. Just a general observation: It seems to me that the proportion of potential amino acid sequences which are "functional" is not something that can be calculated. It is only something that can be estimated from empirical observations and, even then, only very, very approximately. We just have no way of knowing all the possible functions a protein could perform in every single possible context.

      Make sense?

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    33. lutesuite
      "No, human population remains completely irrelevant. You need to know the number of potential winning tickets that are being held. What if they were giving tickets away for free, and everyone on earth decided to get a billion tickets each. Wouldn't that affect your calculation of the odds of someone winning?"

      Not really, lutesuite. One billion tickets each improves the odds of winning to 1/10^31 or about zero. If we increase the number of balls to 69 with 10 numbers per ball then the odds of a winner with everyone on earth having a billion tickets is the same as 1 ticket winning with 50 balls and 10 numbers per ball. Human proteins average of 20^500 possible ways to arrange. This is a real hard mathematical problem for TOE. The mechanism that forms functional DNA sequences is one of the great mysteries of science, right there with the origin of matter.

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    34. lutesuie
      "Oh, I'm sure he did some random calculations to come up with some bullshit number. But, if you think his number has any relevance to real world situation, kindly explain the rationale here."

      I have not gone into his methods enough to understand the possible errors in his calculations but his paper is peer reviewed and so I think there are in the ball park. In discussion with Art Hunt he questions how Axe set the base line of the starting sequence and that he did not assay the enzymes. I think his first point may have merit but disagree with him on the second. I think that the ability of e coli to survive is more relevant to evolution then an arbitrary enzyme frequency measurement.

      You also need to realize that these experiments are on bacterial enzymes and not eukaryotic nuclear proteins which are more likely to be sensitive to AA substitutions as they need to bind to multiple molecules.

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    35. Bill,

      You have a touching faith in peer review.

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    36. Lutesuite
      "Just a general observation: It seems to me that the proportion of potential amino acid sequences which are "functional" is not something that can be calculated. It is only something that can be estimated from empirical observations and, even then, only very, very approximately. We just have no way of knowing all the possible functions a protein could perform in every single possible context.

      Make sense?"

      Yes, I think this is a valid point.

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    37. @ Bill Cole

      Not really, lutesuite. One billion tickets each improves the odds of winning to 1/10^31 or about zero. If we increase the number of balls to 69 with 10 numbers per ball then the odds of a winner with everyone on earth having a billion tickets is the same as 1 ticket winning with 50 balls and 10 numbers per ball. Human proteins average of 20^500 possible ways to arrange. This is a real hard mathematical problem for TOE. The mechanism that forms functional DNA sequences is one of the great mysteries of science, right there with the origin of matter.

      Nice job of missing the point. I have no idea whether your calculations are correct but, if so, just increase the number of tickets purchased per person to a trillion, or decillion, or googol to the googol plexth power, or whatever is needed to make the odds of someone winning a reasonably probabable. The point, in case you still don't get it, is that your analogy is meaningless unless you can demonstrate that your numerator is an accurate reflection of what actually exists in nature.

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    38. @ Bill Cole

      Yes, I think this is a valid point.

      Good. So, since that point refutes your entire line of argument, we're done here. Right?

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    39. I think that the ability of e coli to survive is more relevant to evolution then an arbitrary enzyme frequency measurement.

      Yes. So how did Axe determine the ability of the organism to survive in his mathematical models?

      Delete

    40. "Yes, I think this is a valid point.

      Good. So, since that point refutes your entire line of argument, we're done here. Right?"
      You gotta be kidding me :-)

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    41. lutesuite
      "Yes. So how did Axe determine the ability of the organism to survive in his mathematical models?"

      His base line was a sequence that allowed e coli to reproduce.

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    42. lutesuite
      Nice job of missing the point. I have no idea whether your calculations are correct but, if so, just increase the number of tickets purchased per person to a trillion, or decillion, or googol to the googol plexth power, or whatever is needed to make the odds of someone winning a reasonably probabable. The point, in case you still don't get it, is that your analogy is meaningless unless you can demonstrate that your numerator is an accurate reflection of what actually exists in nature."

      You are missing the point, Lutesuite. A sequence of above 10^120 is greater then the age of all the atoms in the universe in pico seconds. Sequences surpass all the resources in the universe orders of magnitude less than the average number of ways to arrange a human protein. I know this seams bizarre but I will work you through the mathematics off line if you want.

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    43. Lutesuite
      You can get a reasonable estimate of the numerator through experiment as Axe did. There is undoubtedly error in his estimates but not enough to but the argument aside.

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    44. @ Bill Cole

      You gotta be kidding me :-)

      Nope. Dead serious. If you're smart enough and not blinded by your faith, you'll realize this if you think it thru.

      His base line was a sequence that allowed e coli to reproduce.

      That is incorrect. He only attempted to investigate the ability of an enzyme to function as a beta-lactamase. Maybe you don't really understand the paper at all.

      You are missing the point, Lutesuite. A sequence of above 10^120 is greater then the age of all the atoms in the universe in pico seconds. Sequences surpass all the resources in the universe orders of magnitude less than the average number of ways to arrange a human protein. I know this seams bizarre but I will work you through the mathematics off line if you want.

      No need. I know the denominator is a really big number. And creationists' minds are so easily boggled by really big numbers. But, again, with no accurate determination of the numerator, the size of the denominator tells you nothing.

      You can get a reasonable estimate of the numerator through experiment as Axe did. There is undoubtedly error in his estimates but not enough to but the argument aside.

      No, you can't. Not unless you think that beta-lactamase activity associated with only a narrow range of possible enzyme structures (and disregarding all the other, less closely related, structures that can perform the same function) is the only function that any cell performs. Do you think this?

      Delete
    45. Lutesuite
      "No, you can't. Not unless you think that beta-lactamase activity associated with only a narrow range of possible enzyme structures (and disregarding all the other, less closely related, structures that can perform the same function) is the only function that any cell performs. Do you think this?"

      When a bacteria is infected with penicillin it has few choices for survival. So it needs a precise enough sequence to break up penicillin. Proteins need to work together and again the more functions they have the more precise the sequence needs to be or DNA would not be required to create protein sequences.
      Doug's number of 1/10^77 is massively smaller then all the possible sequences that exist in the 20^153 of search space. So his claim mathematically is there are lots of possible arrangements that can create the required enzymic reaction to this specific molecule.

      I know that most nuclear proteins are very sensitive to mutation an thats partially why we have so many diseases like cancer. Sequence integrity matters, and sequential space is really large. How evolution manages this problem is a big mystery.

      Delete
    46. Sequence integrity matters, and sequential space is really large. How evolution manages this problem is a big mystery.

      Good grief, you still banging this drum? You know you will never receive an answer that satisfies you. Why bother the internet with it?

      Delete
    47. Bill Cole says When a bacteria is infected with penicillin....

      It is possible that this sentence provides a clue that you don't know a whole lot about cell or molecular biology.

      Delete
    48. Doug's number of 1/10^77 is massively smaller then all the possible sequences that exist in the 20^153 of search space.

      And, for all practical purposes, is entirely fictitious. He just pullled it out of his ass because he thinks it proves God exists. I know you've read Arthur Hunt's article explaining this; you keep citing it. So clearly you don't understand that article.

      Delete
    49. Anyway, Bill, you still haven't addressed the issue I raised. Sure, if bacteria are exposed to penicillin then beta-lactamase is very immportant to survial. But only a very small portion of E. coli will ever be exposed to penicillin. So beta-lactamase is not required for survival.

      Delete
    50. I think I realize one thing that might be confusing you, Bill Cole. You keep using the analogy of a lottery with 20^150 possible numbers that can be drawn (or some similarly Really Big Number) as an argument against the likelihood of functional proteins arising thru random mutations. But, obviously, this only holds if just a single winning number is drawn.

      Answer me this: Imagine two different lotteries. In the first, there are 1000 possible numbers that can be drawn, and only one winning number is drawn. In the second there are 1 million, possible numbers, but 1000 winning numbers are drawn, and a ticket holder wins if he matches any one of these.

      If you could buy a ticket for one of these lotteries, which would you choose? Which gives you the higher odds of winning?

      Delete
    51. Good grief, you still banging this drum? You know you will never receive an answer that satisfies you. Why bother the internet with it?

      A grateful internet thanks you, Allan.

      Delete
    52. Maybe you don't really understand the paper at all.

      I think you can remove the "maybe."

      On the other hand, the experiment wasn't set up in such a way that its relevance to the way evolution actually works is evident, so perhaps Bill can be forgiven.

      Delete
    53. lutesuite
      And, for all practical purposes, is entirely fictitious. He just pullled it out of his ass because he thinks it proves God exists. I know you've read Arthur Hunt's article explaining this; you keep citing it. So clearly you don't understand that article."

      If you believe this than we don't have any reason to continue.

      I believe that both Axe and Szostak are trying to do good scientific work. If you read Hunts paper I believe that Art believes that Axe is trying to do good work even if he does not agree with all his assumptions. He agrees that Axe's results fall in the range of other papers on the subject. The difference in the ranges he believes are patricianly based on how the measurements were taken.

      There is a difference in the results and that is an interesting point of discussion.

      Delete
    54. The difference in the results is explained simply by the fact that there is no accurate way to determine the proportion of possible amino acid sequences that are "functional". For Axe to build an argument for the existence of God on such a flimsy foundation is a project doomed to failure.

      I look forward to your answers to the other questions I have asked above.

      Delete
    55. Bill Cole, I agree that the authors you cite are trying to do good work. However, some of them are seriously wrong. You'd do well to learn about that if you're going to cite those papers.

      Delete
    56. I think Axe is trying to good work. Just not good scientific work. His goal is Christian apologetics.

      Delete
    57. Lutesuite
      "The difference in the results is explained simply by the fact that there is no accurate way to determine the proportion of possible amino acid sequences that are "functional".

      So you discount Szostak's paper also?

      "Anyway, Bill, you still haven't addressed the issue I raised. Sure, if bacteria are exposed to penicillin then beta-lactamase is very immportant to survial. But only a very small portion of E. coli will ever be exposed to penicillin. So beta-lactamase is not required for survival."

      This is a very inaccurate characterization of the situation.

      " Answer me this: Imagine two different lotteries. In the first, there are 1000 possible numbers that can be drawn, and only one winning number is drawn. In the second there are 1 million, possible numbers, but 1000 winning numbers are drawn, and a ticket holder wins if he matches any one of these.


      If you could buy a ticket for one of these lotteries, which would you choose? Which gives you the higher odds of winning?"

      This is how the math works if I understand you question correctly. 10^-3 is = to 1/10^3

      First case P =10^-3
      Second case P= 10^-6 x 10^3=10^-3

      Delete
    58. BWilson
      Bill Cole,
      "I agree that the authors you cite are trying to do good work. However, some of them are seriously wrong."

      Can you factually back up this claim?

      Delete
    59. Lutesuite
      "I think Axe is trying to good work. Just not good scientific work."

      Can you back up this claim? How is his 2004 paper not good scientific work?

      Delete
    60. So you discount Szostak's paper also?

      I'm not familiar with that paper. Does he try to use it to prove God does or doesn't exist?

      This is how the math works if I understand you question correctly. 10^-3 is = to 1/10^3

      First case P =10^-3
      Second case P= 10^-6 x 10^3=10^-3


      So answer the question: Which lottery gives you better odds?

      This is a very inaccurate characterization of the situation.

      Where am I wrong? Are most E. coli exposed to penicillin? Is beta-lactamase necessary for survival in all situations?

      Delete
    61. Can you back up this claim? How is his 2004 paper not good scientific work?

      That's what is being explained to you.

      Delete
    62. So far as I know, both the Szostak and the Axe paper only assayed for one function. I do not know, biologically, how you can assay for all possible functions.

      Of course you could just measure overall gains in fitness, which would be a measure of all functions detectable in a particular organism in a particular context, at least within one network of interactions, anyway.

      Delete
    63. My point is, I don't think the "Lottery Winner" fallacy is relevant, or more properly, it is equally relevant to both papers.

      Delete
    64. Lutesuite

      "Can you back up this claim? How is his 2004 paper not good scientific work?

      That's what is being explained to you."

      Really?

      Delete
    65. Lutesuite
      "Where am I wrong? Are most E. coli exposed to penicillin? Is beta-lactamase necessary for survival in all situations?"

      You have 4 billion in your gut. Have you ever taken penicillin or a derivative?

      Delete
    66. Or, should I say, questions. There are a number you have ignored in favour of posting irrelevancies.

      Delete
    67. Diogenes
      "My point is, I don't think the "Lottery Winner" fallacy is relevant, or more properly, it is equally relevant to both papers"

      I agree. The lottery discussion is only relevant when population of winners approaches the number of possible combinations.

      Delete
    68. Lutesuite
      "Now answer my question."
      Without the beta-lactamase enzyme in e coli you would be dead. Yes, it has effected very large populations and so your original assumption is wrong. For you lottery question see above.

      Delete
    69. Without the beta-lactamase enzyme in e coli you would be dead

      Sorry, what?

      Yes, it has effected very large populations and so your original assumption is wrong.

      What assumption are you talking about.

      For you lottery question see above.

      You haven't answered it. Which lottery gives you better odds of winning? I don't feel I can assume you know the answer from what you wrote above.



      Delete
    70. Bill, I haven't been following the details of your argument with lutesuite, but it is certainly untrue that "the lottery discussion is only relevant when population of winners approaches the number of possible combinations." The population of winners is the numerator, the number of possible combinations is the denominator. In a fraction, they're both relevant.

      My point is that both Szostak and Axe only tested for a single function. Not all functions. Szostak tested for one function and Axe tested for another. The number of possible functional solutions (numerators) could be different for Szostak's assay vs. Axe's assay.

      If you want to switch to discussions of "all possible functions", you would need to multiple up Axe's result by one number, and Szostak's result by a different number. The fudge factors would be different because they assayed different functions. How much different, I don't have a clue. But the general "lottery winner" problem is relevant to both experiments.

      Delete
    71. Diogenes,
      "Bill, I haven't been following the details of your argument with lutesuite, but it is certainly untrue that "the lottery discussion is only relevant when population of winners approaches the number of possible combinations." The population of winners is the numerator, the number of possible combinations is the denominator. In a fraction, they're both relevant."

      Both are relevant until denominator becomes much larger than the numerator and the fraction approaches zero. Since the growth of the denominator in the lotto discussion is logarithmic this happens very rapidly as sequences increase quickly surpassing the resources available to evolution.

      " If you want to switch to discussions of "all possible functions", you would need to multiple up Axe's result by one number, and Szostak's result by a different number. The fudge factors would be different because they assayed different functions. How much different, I don't have a clue. But the general "lottery winner" problem is relevant to both experiments."

      Interesting point: Need to think this over. Are you defining all possible functions as a fold that performs any enzyme function or any protein function? Is binding ATP a function or something a protein does in order to perform a function?

      Delete
    72. lutesuite
      "You haven't answered it. Which lottery gives you better odds of winning? I don't feel I can assume you know the answer from what you wrote above."

      10^-3=10^-3
      The same odds: It does not matter which game you pick.

      Delete
    73. 10^-3=10^-3
      The same odds: It does not matter which game you pick.


      Very good. You get a cookie.

      That's right. Even though the "sequence space" for the 2nd lottery is 1000 times greater than that of the first, the odds of winning remain exactly the same, because the ratio of winning to non-winning numbers is unchanged.

      So can you see what this has to do with your pet argument about the "sequence space" of possible protein structures? It renders your argument completely irrelevant. The size of the sequence space makes no difference in terms of how likely it is to "find" functional proteins thru random mutations, because the number of possible functional proteins increases proportionally. At least, there is no reason to suppose it does not.

      This is the error you make in your response to Diogenes just above. You assume that, as the number of possible sequences increases, the denominator increases, but the numerator remains the same. That is a false assumption. It assumes that mutations are seeking to "find" a particular sequence (such as that of the beta-lactamase), rather than just any sequence that serves any function.

      As it happens, the larger number of sequences actually makes it more likely to find functional sequences, but that's a different topic. I hope your error is now clear to you, and you will cease to use this fallacious argument.

      Delete
    74. @ Diogenes:

      Bill, I haven't been following the details of your argument with lutesuite...

      You're not the only one. Do you have any idea what Bill was getting at with his claim that I'd be dead if not for E. coli possessing beta-lactamase?

      Delete


    75. Pedantry alert.

      No, the odds aren't the same. In this particular case they're very close, but the odds in the first lottery (1000 numbers, 1 pick) are very slightly better than those in the second (1,000,000 numbers, 1000 picks).

      The second lottery is properly calculated as 1-(1-10^-6)^1000.

      Here's an intuitive justification. By your math, if there were a million picks, the probability of winning would be 1. But do you think every single number is guaranteed to come up? If so, each number must be picked exactly once, and what do you think are the odds of that?

      Delete
    76. lutesuite
      "This is the error you make in your response to Diogenes just above. You assume that, as the number of possible sequences increases, the denominator increases, but the numerator remains the same. That is a false assumption. It assumes that mutations are seeking to "find" a particular sequence (such as that of the beta-lactamase), rather than just any sequence that serves any function."

      How do you evolve a living organism when you evolve a group of proteins with no specific function?

      Delete
    77. John
      "Here's an intuitive justification. By your math, if there were a million picks, the probability of winning would be 1. But do you think every single number is guaranteed to come up? If so, each number must be picked exactly once, and what do you think are the odds of that?"

      Very good: My assumption was that once a number was picked it was not replaced.

      Delete
    78. lutesuite
      "So can you see what this has to do with your pet argument about the "sequence space" of possible protein structures? It renders your argument completely irrelevant. The size of the sequence space makes no difference in terms of how likely it is to "find" functional proteins thru random mutations, because the number of possible functional proteins increases proportionally. At least, there is no reason to suppose it does not."

      I think this assumption is speculative at best and almost certainly wrong.

      Delete
    79. Very good: My assumption was that once a number was picked it was not replaced.
      Possibly a good assumption for a lottery, but a poor assumption for the analogy.

      Delete
    80. How do you evolve a living organism when you evolve a group of proteins with no specific function?

      Not "no specific function". Some function that's advantageous at the time. You are again assuming that there is one specific target sequence.

      Delete
    81. John
      "Not "no specific function". Some function that's advantageous at the time. You are again assuming that there is one specific target sequence."

      I am not assuming this, I am claiming that there is a group of functions that may help give advantage to the organism but that a new protein must work with other molecules in the cell to help gain advantage. Just binding to ATP is not enough.

      In the case of multi protein complexes like a ribosome each protein evolved must bind to a specific protein for the system to function. This is grossly underestimating the requirement because of the very complex function of the system i.e. translating RNA sequences to AA sequences.

      Delete
    82. A ribosome isn't a multi-protein complex. It's RNA that has a lot of proteins around it to improve its function. The RNA can do the job all by itself. So that system is easily improvable in small increments: new protein here, improved protein there.

      "Binding ATP" is just one function, chosen for no particular reason. Do you have any evidence that most other functions are less common in random sequences?

      Delete
    83. "
      "Binding ATP" is just one function, chosen for no particular reason. Do you have any evidence that most other functions are less common in random sequences?"
      From Axe's paper it appears that an enzyme function is more sequence specific then binding ATP. This is backed up by other papers in Hunt's article. There is variation depending on the enzyme but all cases above the ATP binding data.

      The other evidence is the sequence sensitivity of nuclear proteins in eukaryotic cells especially those that bind with multiple proteins and involved in the cell cycle. This evidence is supported in cancer research.

      Do you have evidence that the translation process can be supported by RNA alone?

      Do you agree that the evolved proteins in the ribosome need to have specific sequences?

      Delete
    84. Do you have evidence that the translation process can be supported by RNA alone?

      Afraid I don't have a reference handy. But it's true.

      Do you agree that the evolved proteins in the ribosome need to have specific sequences?

      No. I agree that they do have specific sequences, but that's quite another thing. I see no reason to suppose that a completely different set of ribosomal proteins could have evolved, bearing no resemblance to the ones we see.

      Delete
    85. Bill, let's clarify what you're doing wrong. In response to me saying "The population of winners is the numerator, the number of possible combinations is the denominator. In a fraction, they're both relevant," you replied

      Both are relevant until denominator becomes much larger than the numerator and the fraction approaches zero.

      This is very wrong. The numerator is always important to the actual value of the fraction, obviously. However, you seem to be focusing not on the value of numerator/denominator but rather for the overall behavior as the sequence gets longer (L= length increases). Why do you think this? Because you think that, as the sequence gets longer, the numerator [number of possible functional sequences] becomes a constant independent of L while the denominator [number of randomized sequences] explodes combinatorially or exponentially in L.

      "Since the growth of the denominator in the lotto discussion is logarithmic this happens very rapidly as sequences increase quickly surpassing the resources available to evolution."

      Actually the growth of the denominator would be exponential in L or factorial in L depending on the details of the draw. This is not the problem, the problem is your assumption that the numerator becomes independent of L.

      Lutesuite points out, correctly I think, that both the numerator and denominator will increase exponentially or factorially in L as length increases. Of course the numerator will always be smaller than the denominator. The ratio could go down... or up. It's not obvious. You believe the ratio must approach zero because you assume without evidence that the numerator approaches a constant.

      The problem with this is that you ignore that the number of functional sequences will also increase combinatorially. The longer the sequence is, the more possible sequences can carry out a function.

      Delete
    86. Continuing: Let's think about real world proteins. When you align a family of sequences, you find that some of the amino acids-- typically a minority-- are "conserved" and you can't monkey with them without affecting function, while the rest-- typically the majority-- can be mutated without killing function.

      (Some people on this website disagree with my "majority can be mutated safely" rule but I'm telling you this is what most sequence alignments look like, and it's the working experience of the molecular biologists I know that if they mutate a randomly chosen residue, most of the time it does not kill function. If it does, that's "bad luck" meaning the exception to the rule.)

      Now what is the fraction of conserved to unconserved? Depends on the family of proteins, of course. I'd say it's typical to see 1/3 of residues conserved and 2/3 tolerant to variation. Some will argue, and there are wide variations. It is rare to see a family where 2/3 are conserved and 1/3 tolerant to mutation. It happens, but it's rare.

      So, for illustrative purposes, let's assume pessimistically that 1/2 the residues are invariant and 1/2 tolerant to mutations in a sequence of length L.

      If that's true, then, given this fixed protein fold, how many sequences would carry this function? At least 20^(L/2). If you pick some other fraction of invariant residues, say f, so 1-f is the fraction of residues tolerant to mutation, then the number of sequences that carry this function would be at least 20^(L*(1-f)). This assumes: 1. we're limited to this fold, ignoring other folds that could also do this function, and 2. the non-invariant amino acids are individually totally variable and not interdependent. (This second assumption might be invalidated by complex interactions between double mutants, etc.)

      But the point is, the numerator goes exponentially in L. You know the denominator goes exponentially in L too, something like 20^L. So the ratio would be like:

      20^(L*(1-f))/20^L = 20^(L*(1-f)-L) = 20^(-L*f) = 1/20^(L*f)

      Recall f < 1 so this is a small number. But the point is, the numerator does not approach a constant, so you can never ignore it. If f=1/3 then

      20^(L*(1-f))/20^L = 1/20^(L/3)

      This increases with L, but more slowly.

      But these assumptions are not so realistic: the above assumes that the number of invariant residues increases with L. This is unlikely in the real world. In real world protein families, the invariant residues are usually 1. those involved in the functional site and 2. those involved in the hydrophobic core of the protein (surface, non-functional residues are highly variable.)

      Now, I've looked at and analyzed hundreds of protein functional sites, and I'm telling you that their size is primarily determined by the size of the substrate, not by the size of the protein. E.g. if the function is to bind a metal ion, the functional site will be about the same size in big and small proteins that bind that metal (a caveat: big metal-binding proteins often have more, equally sized binding sites.) But my subjective experience is that functional sites don't get bigger as the protein gets bigger, they get bigger as the substrate gets bigger. The smallest functional sites are metal binders, the largest are DNA binders.

      This means that the total number of invariant residues should be approximately constant as the sequence gets longer, assuming the function does not change and there are not multiple functions or functional sites. Thus the fraction of residues tolerant to mutation should go up as L increases. If we assume the functional site has a fixed size S, and all its residues are invariant, the numerator would be more like 20^(L-S), and the fraction would be like:

      20^(L-S)/20^L = 1/20^S

      which, I'll note, is independent of L. This is an extreme case but it's not unrealistic. This emphasizes that you cannot ignore the numerator as the denominator increases.

      Delete
    87. There has also been discussion about whether enzymatic activity is more sequence specific than ATP binding. There is no good reason to assume this, because enzymatic functions are also a kind of binding, they bind to an intermediate state in a reaction. Here is how enzymes (or catalysts in general) work. Suppose a molecule X would turn into Y spontaneously because Y has less free energy than X. But, it must go through an intermediate state X' that has more free energy than X-- so X' is an energy hill that must be climbed over to reach Y.

      An enzyme (or any catalyst) simply binds X' and reduces its entropy thus reducing its free energy or stabilizing it, so the substrate can now tunnel through the energy hill. Since catalysis IS a kind of binding, there is no reason to believe it requires more invariant residues.

      The most famous catalytic site is the "catalytic triad" of proteases, with just 3 amino acids to perform the function-- although, since most proteases are specific to certain protein substrates, there are typically additional residues around the catalytic triad, which exclude undesired substrate molecules from binding. But 5 or 6 invariant residues is totally doable for a protease or general hydrolase functional site.

      Delete
    88. I've pointed this out to Bill before, evidently to no avail, but this whole argument, starting with a 20-acid space, implies that, if a small functional peptide with few acids were the starting point, its evolution by extension in either dimension - length or acid library - slows to a halt because the 'space' it inhabits grows massively with each added dimension. That is, the more subfunctionalisation, kinetic tuning and conformational subtlety available to proteins, the less they can evolve. This is clearly nonsense.

      Delete
    89. I've also pointed out that, at many sites, the correct number for 'acid library' can be as little as 1. Using 20 for every site while ignoring this redundancy shows a fundamental, apparently uncorrectable misunderstanding of the grouping of chemical properties, and the effect of neighbourhoods in the folded peptides. The anticipated response will be to point again to Szostak and Hunt's papers. Without wondering why they don't consider protein evolution to be impossible.

      Delete
    90. lutesuite
      "So can you see what this has to do with your pet argument about the "sequence space" of possible protein structures? It renders your argument completely irrelevant. The size of the sequence space makes no difference in terms of how likely it is to "find" functional proteins thru random mutations, because the number of possible functional proteins increases proportionally. At least, there is no reason to suppose it does not."

      I think this assumption is speculative at best and almost certainly wrong.


      "Almost certainly"? I'd like to see the evidence upon which you base that.

      I guess the argument you're trying to make is analogous to this: If you're holding a lottery ticket with the number 999, then your odds of winning are greater if the possible numbers to be drawn are limited to those between 1 and 1000, as opposed to those between 1 and 1,000,000.

      But what if the number you hold is 1001? Oh no, now what?

      Delete
    91. diogenes
      "Both are relevant until denominator becomes much larger than the numerator and the fraction approaches zero.

      This is very wrong. The numerator is always important to the actual value of the fraction,"

      You are not reading my statement accurately and therefor arguing against a straw-man.

      I will read the rest of your posts by tomorrow and respond to you Allan and Lutesuite.

      Delete
    92. Does anybody have a copy of the Axe 2004 paper that they can email me? It's behind a pay wall, but I want to find out where his math went wrong.

      Delete
  2. On the bright side Larry: Donald Trump is doing such a fantastic job of destroying Mike Pence's political career that the election is actually going very well, for science.

    ReplyDelete
    Replies
    1. I have to agree with you here, Gary.

      If a delusional religious zealot (= anti-science) like Pence is scuttled by this farce of an election run by Donald, I would definitely consider it a 'bright side'.

      Delete
    2. You're assuming Trump looses. He should loose. He probably will loose. I certainly hope he looses. But in this weird election I'm afraid we won't know until November.

      Delete
  3. A little disappointing to hear on this blog that being creationist, one and all I guess, makes one anti-science. !
    I thought we were beyond that.
    I don't agree there was the mythical stone age but its been going that way since AFTER Reagan. step by step. no better in Canada.
    At least, hopefully, origin issues will matter in this eclection as they should. Ending state censorship on origin matters is all anyone in poltics should be concerned about .

    ReplyDelete
    Replies
    1. Robert,
      Please spare me the drama. YECs are by definition anti-science. And as a scientist, I don't say such things casually. I abhor absolutes. But to be a YEC, one has to be so self deluded and in denial of established scientific facts that others must question the YEC's ability to think rationally. Folks like Michael Pence should not be in any position of authority, because they are making decisions based on their religious fantasies. Cruglers above is an example.

      It is a sad situation when someone like Cruglers can emit such factually inaccurate nonsense and be lauded for it, while an atheist is essentially disqualified from elected positions if it should be revealed that they don't believe in a god (given that there is no evidence for such a creature).

      Delete
    2. Evolutionary Creationists are "Creationists" too. Someone like Larry who believes that we were caused by the common ordinary behavior of matter sees that as how they were created, which in my opinion qualifies as their "creator".

      With the now relatively useless labels aside: the issue is over things like using scripture to support "scientific theories" that do not even explain why uplift is expected to force the most deeply buried and oldest sediments to a higher altitude. Tactics like the using of excellent evidence for uplift to support a theory that assumes the fossils were formed right there on the mountain is a good indication of a very tragic public science education problem, being made worse by politicians and other leaders who have no interest in what is going on at my tracksite and elsewhere in science.

      More here:
      http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?act=ST;f=14;t=7420;st=17010#entry254162

      Delete
    3. I don't agree there was the mythical stone age

      I usually resist temptation, but Robert, I have to ask: If the Stone Age was mythical, where did all those, y'know, *stones* come from with marks from people working on them?

      Delete
    4. Chris B. well call us irrational but not anti-science. We could love and embrace'science" but just do a bad job including irrationality as a handicapp!
      We don't reject establish facts. We take on whether facts are established. lots of thinkers in science did this right oir wrong in the end.
      From my reading of scientific accomplishments its ABSOLUTELY the lesson to take on existing paradigms and so called facts.
      Its absolutely true the winners did and do this. few worked within settled conclusions.

      Delete
    5. Judmaree.
      Any worked stone tools was done in early migrations or the lower classes of these rough and ready early settlements of mankind.
      the stone age is a fable based on the presumption of a evolving intelligence in man.
      Never did this happen . It must be admitted mans inteklligence was so great it would never be stuck for a while unable to think up better ideas then stone tools.
      Many human societies did use stone tools but it would only be special cases of not having other materials. not a evolving ability to move on being not yet there.

      Delete
    6. Byers:"We don't reject establish facts."

      Of course you do. You absolutely reject the established fact from DNA and other molecular evidence that shows that thylacines are more closely related to kangaroos than to wolves.

      Delete
    7. Christine Marie Janis
      I reject the dna is accurately interpreted. The common adaption of marsupialism would be common in the dna of all marsupials.
      So if one accepts its from a triggering event after migration to a area etc etc then all marsupials would have like dna to account for the marsupialism traits.
      For scoring it I could suggest this late reaction to marsupialism has a reaction in the dna to dominate it. something like that.
      The dna is following the physical traits and not a trail of comon descent. Then, i think, late modeling actions make it top heavy in reading the dna.

      Delete
    8. Byers says: "I reject the dna is accurately interpreted. The common adaption of marsupialism would be common in the dna of all marsupials. So if one accepts its from a triggering event after migration to a area etc etc then all marsupials would have like dna to account for the marsupialism traits."

      Byers' published hypothesis is that marsupial mammals are just placental mammals that swam to Australia after Noah's Flood, then something in the Australian environment (totally unspecified) changed them and their offspring into marsupials. This is what he means when he says "a triggering event after migration to a area etc etc." He does not explain what the "event" is. Magic marsupial rays sent out by Ayers Rock?

      According to Byers, there are marsupial versions of every placental, so he has claimed the existence of weird things like "Placental horses" which go unobserved and unexplained.

      Also unexplained is how humans, rabbits, etc. today resist being turned into marsupials by Australia's "marsupial rays."

      Of course Byers' cannot explain the suite of homologous features which characterize marsupials, for example, the two holes in the palate of their moves, their dental patterns, and so on.

      Real paleontologist Kevin Padian demolished creationist arguments against homology as evidence for evolution with a detailed description of homology and convergent evolution in marsupials vs. placental mammals during his testimony at the Intelligent Design Trial in Dover. Read the link if you haven't, it's detailed but good.

      Delete
    9. P.S. Byers needs to show that the massive, overwhelming DNA similarity between thylacines and kangaroos is entirely functional in nature (not due to common descent of thylacines and kangaroos) and due to Byers' alleged "triggering event" that can turn any placental mammal into a marsupial, except not humans nor rabbits for some unknown reason.

      Byers needs to show that ALL the DNA similarites are functional. Of course, he has never even taken a peek at even one nucleotide from one gene of any marsupial anywhere. It's all bluffing.

      Delete
    10. Any worked stone tools was done in early migrations or the lower classes of these rough and ready early settlements of mankind.

      And what were the dates of these settlements, Robert? Do you reject the radiocarbon dating saying it was in some cases millions of years ago? That's based on radioactivity, so do you reject radioactivity? If not, next time you get a dental X-ray, are you gonna ask them not to bother with that stupid lead bib?

      Delete
    11. 'Also unexplained is how humans, rabbits, etc. today resist being turned into marsupials by Australia's "marsupial rays." '

      Not to mention the native Australian rodents, which have been there for about 5 million years, and all of the marsupials in South America living alongside a large diversity of placentals that also evolved there,

      Delete
    12. Also, you might like to read about how the "marsupial lion" wasn't really lion-like at all in its behavior

      http://paleobiol.geoscienceworld.org/content/42/3/508

      Delete
    13. And why didn't the monotremes turn into marsupials?

      Delete
  4. This is far from the only anti-science stance of Pence. He believes abortion drugs are extremely dangerous, that scientists are "actively debating and doubting" climate change, and that there is not a link between smoking and cancer, believes "gay conversion therapy" works and believes the government should fund "institutions that want to use it to help people".

    I have a feeling that if he were to be scratched there would be much more evidence of his vile nature exploding from the wound.

    ReplyDelete
    Replies
    1. Do you happen to have a source for Pence claiming no link between smoking and cancer? I would like to share that with some folks.

      Delete
    2. http://thinkprogress.org/politics/2016/07/14/3798417/mike-pence-tobacco-money/

      Delete
    3. That is alarming.

      Compared to his stance on various aspects of human rights, and whose vice president he's willing to be, I'd consider the usual lying-for-money stuff like this to be chicken feed.

      Delete
  5. People need to understand that the theory of Evolution has also evolved. We know much more now about DNA and mutations than Charles Darwin knew. Everyone, who still only cites Charles Darwin needs to spend a few days in a lab, experimenting with E.coli to really appreciate the concept of evolution. And they should also study how micro-organisms can acquire resistance to antibiotics. Do creationists acknowledge that there is resistance to antibiotics, and the theories about how this resistance arose?

    We should ask creationist to stop wondering and start studying what humanity has found out in the areas of biology, chemistry, and physics, since Darwin's time.

    Roma

    ReplyDelete
  6. Unfortunately, the Donald and Pence are not the only numbskulls running for POTUS/VICE-POTUS. The Green Party candidate, Dr. Jill Stein, a Harvard educated MD no less, is a vaccine skeptic, a GMO skeptic, and who believes that WIFI may be dangerous. Must be something in the water up there in Cambridge.

    I hope that Canadians are getting a good laugh at the shenanigans going on south of the border. Given the high negatives of the Democratic candidate, Hillary Clinton, it is not out of the realm of possibility that the Donald could win in November.

    ReplyDelete
  7. This upsets me, but I am far more concerned with leaders who secretly try to overthrow foreign leaders (for example, Assad and Qaddafi). Has any good come of that?

    ReplyDelete
    Replies
    1. petrushka
      AMEN. for both. The desire to see them overthrown was greater then the desire to not bring death to people. In syria , not so secret, this has not stoped killing but nurtured it and with all the crazy results ever since.
      I blame all leaders in these matters,Canada, america, France, etc etc.
      The principal of tHOU SHALT NOT MURDER did not prevail. its murder except for self defence or judicial punishment for murder.
      i must say, very cautiously and sadly, it does seem one reaps what one sows.
      With Clinton, Trump, truedeau there seems no hope in these matters.

      Delete
  8. Actually, the revolt against Assad started because of a drought that drove people off the land into the cities. Although the Obama Administration certainly had nothing good to say about the Assad kleptocracy, the US had very little involvement until the rise of the ISIL. The US bombing campaign is targeting ISIL forces, not Syrian Government forces. It's actually the mad mullahs in Iran and their wholly owned subsidiary Hizbollah in Lebanon that are keeping the Assad Government in power. Had they stayed out, Assad would have been overthrown long ago. Currently, it's the Russian intervention against both the ISIL and other anti-Assad forces that are propping him up.

    ReplyDelete
    Replies
    1. Not the thread or the place but that is so inaccurate. Bush was first pushing, and the establishment, to aid the revolt against Assad.
      America, israel, and european nations saw a chance and did all they could to keep the murdering and killing going on for regime change.

      Delete
  9. Lets put it straight:

    Abiogenesis is DEAD.
    the transition from prokaryotes to eukaryotes is DEAD. Impossible
    the transition from unicellular to multicellular organisms is DEAD. Never happened. Energy requirements of eukaryotes make the transition impossible.
    Complex life forms require far more than just genetic, but also epigenetic information.

    Who is still living in a fantasy world created by Charles Darwin ?

    We live in a POST darwinian world, where science has revealed the REAL mechanisms of biodiversity: Preloaded information through intelligence. And from primitive blob of protoplasm , we know now that cells are the most complex super hightech factories in the universe, full of advanced molecular machines, which require a minimal gene set all at once in order to function.

    On which side is the anti science ? I'd say on the side of the ones that desperately grab on refuted views based on poor scientific data and consequently poor understanding of how the natural world works.

    ReplyDelete
    Replies
    1. Otangelo, please explain how the "intelligence" creating the "Preloaded information" works.

      My model looks like this:
      https://theoryofid.blogspot.com/

      Yours?

      Delete
    2. Gary

      "Behavior of matter causes self-assembly of molecular systems"

      Thats just nonsense. Unless you can back up the claim. Can you?

      Delete
    3. I can back up my claims with a self-assembly demonstration that is used by science teachers:
      https://sites.google.com/site/garysgaulin/home/NSTA2007.pdf

      What do you have?

      Delete
    4. Gary
      your paper starts with the title "Demonstrating the
      Self-Assembly of the Cell Membrane". The title starts already with pseudoscientific nonsense. The ENDOPLASMIC RETICULUM cannot exist without the cell membrane. The cell membrane is however sinthesized in the ENDOPLASMIC RETICULUM. You can obviously argue now that the cell membrane of the first organisms did not have to be as complex as they are today. Scientific evidence however does not point to that direction :

      http://www.ncbi.nlm.nih.gov/pubmed/16431085
      the estimate of LUCA's gene content appears to be substantially higher than that proposed previously, with a typical number of over 1000 gene families, of which more than 90% are also functionally characterized.a fairly complex genome similar to those of free-living prokaryotes, with a variety of functional capabilities including metabolic transformation, information processing, membrane/transport proteins and complex regulation, shared between the three domains of life, emerges as the most likely progenitor of life on Earth

      Delete
    5. Otangelo Grasso says,

      The cell membrane is however sinthesized in the ENDOPLASMIC RETICULUM. You can obviously argue now that the cell membrane of the first organisms did not have to be as complex as they are today. Scientific evidence however does not point to that direction :

      Your amazing knowledge of biochemistry continues to astound observers.

      Just out of curiosity, can you explain to me how bacteria like E. coli manage to synthesize a cell membrane without an endoplasmic reticulum?

      Delete
    6. Endoplasmic reticulums are just another self-assembled membrane structure. The only major difference is the membrane self-assembles around the RNA worksite, instead of the outer surface of the cell or other organelle. Whatever becomes most attracted to a membrane ends up part of it.

      If this were as impossible as you make it seem then it would be impossible to shake oil, water and solids into cellular type structures such as vesicles that make your salad oil dressing smooth and creamy. Otherwise you just have a layer of oil, water, while all the solids stay stuck together and never mix in either.

      Basic chemistry happening in restaurants everywhere makes it easy to understand how cell organelles self-assemble then hold their shape. Your need to make even that seem impossible without divine intervention does not bode well for your knowledge of basic chemistry, and whatever belief system is causing you to be so hostile towards science.

      The intelligence responsible for our creation is indeed a very powerful entity that I have much respect for. But that's from many times having modeled what happens when even a very simple system that for molecules can self-replicate even by just water motion becomes able to self-learn. It soon enough figures out how to self-replicate itself then takes over the entire planet. Ultimately even controls its weather and atmosphere.

      I am very willing to discuss biological intelligence with you or anyone. But you'll have to get on the same page as everyone else in science who studies how intelligence works. You are otherwise just another who throws insults instead of helping to SCIENTIFICALLY explain how ANY "intelligent causation" works. Magical thinking is now just a poor excuse for excusing yourself from the real science work needing to be done. So please stop doing that.

      Delete
    7. Otangelo is attempting the old argument, to use an analogy, "To build a road, you need construction trucks. But trucks cannot travel without a road. Therefore, they both must have been created at the same instant in time!" It's silly when minor changes in structure eliminate the mutual interdependence, which is true for all the biological claims he makes.

      And "abiogenesis is dead"? Please. Even in the last few years new results have shown us that ribonucleotides can be synthesized abiotically and that probabilistically accessible, short RNA's can function as catalytic ribozymes. It's an active area of reseach, but "Poof! It happened all at once in a magic puff of smoke!" is not.

      Delete
    8. Larry

      In the book the membranes of cells, we read:

      The active sites of the enzymes for the final stages of lipid biosynthesis in endoplasmic reticulum are all found on the cytoplasmic face of the endoplasmic reticulum (and in E. coli, on the cytoplasmic face of the cytoplasmic (inner) membrane. Ok, so E.Coli does not require the ER. But the outer membrane of E.Coli requires lipopolysaccharide (LPS), which is essential for its survival.

      Furthermore, we read in the paper "Lipopolysaccharide: Biosynthetic pathway and structure modification" :

      The biosynthesis of LPS in E. coli is initiated in the cytoplasm from a small molecule, UDP-N-acetylglucosamine (UDP-GlcNAc). A multiplicity of enzymes sequentially function to convert UDP-GlcNAc into disaccharide-1-P, Kdo2-lipid A, core-lipid A, and culminating in LPS.

      So , the cytoplasm, and the mentioned molecules and enzymes are required. They cannot exist without the cell membrane. This is also a situation of interdependence.

      Chemist Wilhelm Huck, professor at Radboud University Nijmegen
      A working cell is more than the sum of its parts. "A functioning cell must be entirely correct at once, in all its complexity"

      Delete
    9. Diogenes

      http://phys.org/news/2013-09-assumptions-life.html#jCp
      But for the hypothesis to be correct, ancient RNA catalysts would have had to copy multiple sets of RNA blueprints nearly as accurately as do modern-day enzymes. That's a hard sell; scientists calculate that it would take much longer than the age of the universe for randomly generated RNA molecules to evolve sufficiently to achieve the modern level of sophistication. Given Earth's age of 4.5 billion years, living systems run entirely by RNA could not have reproduced and evolved either fast or accurately enough to give rise to the vast biological complexity on Earth today.

      OOL theorist Leslie Orgel notes that an "RNA World" could only form the basis for life, "if prebiotic RNA had two properties not evident today: a capacity to replicate without the help of proteins and an ability to catalyze every step of protein synthesis." The RNA world is thus a hypothetical system behind which there is little positive evidence, and much materialist philosophy: "The precise events giving rise to the RNA world remain unclear … investigators have proposed many hypotheses, but evidence in favor of each of them is fragmentary at best. The full details of how the RNA world, and life, emerged may not be revealed in the near future.

      Delete
    10. Gary wrote:

      "Endoplasmic reticulums are just another self-assembled membrane structure."

      And a boeing 747 can also self assemble, given enough time?

      I have rarely seen someone making worse pseudo scientific just so nonsense claims as you do.

      Delete
    11. I think that God must have done it. He poked the molecules just right with his little finger while hiding behind a bush. Now that the origin of life has been figured out I think it's time for some barbecue! Yeah haw!!!

      Delete
    12. I now feel like I'm arguing with a chatbot, who has a very limited set of responses. And could very well be!

      Otangelo, somehow please prove that you are human.

      Delete
    13. Grasso: "scientists calculate that it would take much longer than the age of the universe for randomly generated RNA molecules to evolve sufficiently to achieve the modern level of sophistication"

      Who are these "scientists"? I really doubt that scientists did any such calculation. Citation please.

      It sounds like creationist shit-- and your statement appears contradictory, "randomly generated RNA molecules to evolve sufficiently..." Are they randomly generated or did they evolve?

      Of course the answer is that they could easily be randomly generated in the early stages of abiogenesis-- certainly a randomly generated library containing an exhaustive search of every possible ribozyme of length 50 is plausible for an abiotic Earth-- and then evolve thereafter.

      If these anonymous "scientists" of yours who "calculate" such a low probability consider a two-step process, first a random library of self-replicators and next evolution-- how the hell do they know what is the level of efficiency of the randomly generated ribozymes? Where'd they get THAT from? Experiment? Theory? Anyway, we know from many experiments that natural selection takes enzymes and rapidly tunes up their fitness. If they're way off from a fitness peak, there are comparatively more beneficial mutations and evolution is faster.

      So how was this calculation calculated? I will check the math.

      Delete
    14. Otangelo you're quote mining prof.Huck, but since your whole attack on evolution and OOL is one big quote mine this isn't a really big surprise...
      You can read about Huck's work on nano medicines, which has nothing to do with OOL. Unfortunately the page is in Dutch, but google translate might help...

      Delete
    15. Grasso first said: "The cell membrane is however sinthesized in the ENDOPLASMIC RETICULUM."

      It was pointed out that bacteria synthesize cell membranes without an ER.

      Grasso: "The active sites of the enzymes for the final stages of lipid biosynthesis in endoplasmic reticulum are all found on the cytoplasmic face of the endoplasmic reticulum (and in E. coli, on the cytoplasmic face of the cytoplasmic (inner) membrane. ... So , the cytoplasm, and the mentioned molecules and enzymes are required. They cannot exist without the cell membrane."

      The last statement is an attempt to save the previous, false statement but is logically irrelevant. So what if the active sites synthesizing the last stages of lipid biosynthesis are in the ER? Why couldn't they have been somewhere else besides the ER in earlier lifeforms?

      And also, how do you know that in early proto-cells, the final stages of lipid biosynthesis were by membrane-bound enzymes? It could have been abiotic catalysts. There are abiotic reactions that create lipids. Here is a list of articles on abiotic lipid biosynthesis.

      Surely you must realize that the early proto-cells would have lipids at least partially syntesized abiotically, then later enzymes would take over.

      I return to my analogy, which you ignored.

      Grasso, why don't YOU explain to us what is wrong with this logic: "To build a road, you need construction trucks. But trucks cannot travel without a road. Therefore, they both must have been created at the same instant in time!"

      So, YOU tell US what's the defect in that thinking. Do you agree it is not logical?

      Delete
  10. Robert said: A little disappointing to hear on this blog that being creationist, one and all I guess, makes one anti-science. !
    I thought we were beyond that.


    I am sorry to disappoint you but you are just as much anti-science as the worst of the creationist crowd. You probably never will learn enough science to intelligently debate with people who's made some effort to learn a little science. I don't know what's the matter with you. Are you living in an intellectual vacuum, with nobody else than yourself to talk to where you live?

    ReplyDelete
  11. So, as predicted/obviously nobody could provide any experimental evidence that swayed they to believe that life originated on its own.

    Let's see the "fantasy evidence" instead. I'm sure it is just as reliable and meets the scientific theory requirements.

    ReplyDelete
    Replies
    1. We could divide the evidence into two groups. First, the millions of experiments in physics, chemistry, biology, geology, etc. that show that interesting things happen without the intervention of some supernatural being or designer or intelligence. That leads one to ask, could life originate the same way?

      In order to have living things like we see on earth today, you need proteins, genetic material (DNA, RNA, or something like that), membranes, ion cascades across membranes, etc. Can these form without some supernatural intelligence?

      Experiments have shown that if you take basic non-living chemicals that must have existed on the early earth (CO2, H2O, N2, NH3, phosphates, etc.), keep oxygen away, and add an energy source (equivalent of lightening or superheated volcanic vents or whatever), and wait, you'll get amino acids, hydrocarbons, phospholipids, nucleotides, and other fairly simple organic compounds. These in turn can (it's been experimentally shown) form more complex forms like polypeptides (short proteins) and RNA. When shaken, the phospholipids form membranes of little vesicles (bubbles; no surprise to anyone familiar with soap). These vesicles can concentrate other organic compounds. Some people are beginning to look into spontaneously occurring, energy-releasing electron flows across simple membranes.

      Does this add up to the formation of a living cell? No. But it does indicate that a lot of the pieces can form spontaneously. More research is going on, slowly. There is every reason to think we'll learn more about this.

      Am I going to go find the citations for this experimental evidence? No. It exists and if you were interested you could find it. Evidence from your comments strongly suggests that you won't pay attention to it anyway, probably because you don't want to believe it exists.

      Delete
    2. Yes bwilson, from experimental evidence it's now possible to conclude that the stuff of life was already abundant in the deep seas to the shorelines. The probability of self-organization into living things (where properly calculated) has a 100% chance of happening on its own and will go as the fossil record shows, by taking it one step at a time to us.

      Following the evidence wherever it leads led to my discovering that I'm physically part of something that has for billions of years been alive by their taking it one lifetime at a time.

      I don't need magical thinking to be awestruck by the intelligent forces that created and are still through us very much alive, too. In religious terms that's spiritual growth by gaining a better understanding of our creation by finding out how the intelligence that leads to our Creator works. It's something that excites a whole other level that seems to get a thrill from at the human intelligence level describing the science of itself/ourselves. Discovering knowledge like this qualifies as a revelation, though not all see insight that help religion forever stay in harmony with science as a future changing "miracle".

      In case Cruglers missed my way of explaining the basic chemistry:
      http://originoflifeaquarium.blogspot.com/

      With the US youth now into BattleBots that are already capabable of some remarkable dance moves it's as though a new world that leads to a better understanding of ourself has begun, even though it's rather primal battling, as opposed to watching robotic intellectuals at least as smart as we are having a go at it.

      Delete
    3. Cruglers, at this point you're consciously lying. You made broad statements that there was no evidence for endosymbiosis, which presupposes that you have encyclopedic knowledge of the topic.

      I showed that there was evidence, which means either that you knew there's evidence and lied about it not existing, or your misrepresented your alleged encyclopedic knowledge of the topic.

      Now you return to mere repetition of denials-- "as predicted/obviously nobody could provide any experimental evidence that swayed they to believe that life originated on its own"-- as if by repeating falsehoods many times you will exhaust us. This strategy is far too common.

      Delete
  12. Digoenes wrote:

    Of course the answer is that they could easily be randomly generated in the early stages of abiogenesis-- certainly a randomly generated library containing an exhaustive search of every possible ribozyme of length 50 is plausible for an abiotic Earth-- and then evolve thereafter.

    First of all: Since when has chance the goal of " exhaustive search " ? Chance has no purpose, no goal. Randomness isn't something, nor does it generate instructed complexity as required to produce replication. According to Wiki : "Randomness is the lack of pattern or predictability in events". Thats exactly what precise replication requires.

    Paul Davies The Algorithmic Origins of Life
    Despite the conceptual elegance of the RNA world, the hypothesis faces problems, primarily due to the immense challenge of synthesizing RNA nucleotides under plausible prebiotic conditions and the susceptibility of RNA oligomers to degradation via hydrolysis 21 Due to the organizational structure of systems capable of processing algorithmic (instructional) information, it is not at all clear that a monomolecular system – where a single polymer plays the role of catalyst and informational carrier – is even logically consistent with the organization of information flow in living systems, because there is no possibility of separating information storage from information processing (that being such a distinctive feature of modern life). As such, digital–first systems (as currently posed) represent a rather trivial form of information processing that fails to capture the logical structure of life as we know it.

    We need to explain the origin of both the hardware and software aspects of life, or the job is only half finished. Explaining the chemical substrate of life and claiming it as a solution to life’s origin is like pointing to silicon and copper as an explanation for the goings-on inside a computer. It is this transition where one should expect to see a chemical system literally take-on “a life of its own”, characterized by informational dynamics which become decoupled from the dictates of local chemistry alone (while of course remaining fully consistent with those dictates). Thus the famed chicken-or-egg problem (a solely hardware issue) is not the true sticking point. Rather, the puzzle lies with something fundamentally different, a problem of causal organization having to do with the separation of informational and mechanical aspects into parallel causal narratives. The real challenge of life’s origin is thus to explain how instructional information control systems emerge naturally and spontaneously from mere molecular dynamics.

    Systems of interconnected software and hardware like in the cell are irreducibly complex and interdependent. There is no reason for information processing machinery to exist without the software, and vice versa.

    Diogenes wrote : " Anyway, we know from many experiments that natural selection takes enzymes and rapidly tunes up their fitness."

    We are trying to elucidate and explain the origin DE NOVO of functional proteins and enzymes, not their evolution.

    ReplyDelete
    Replies
    1. I would like to know what Joe Felsenstein thinks of the following.

      Grasso's quote above is a terrible passage, because for one thing, I can't tell where Davies ends and Grasso takes over. But the first passage is incoherent, because "mechanical aspects" is not defined-- at least not within the passage-- what are "mere molecular dynamics"? I would want a mathematical definition of "mechanics" of life as well as "information."

      Note there is no definition of "information" in this passage. Creationists never give us an equation for measuring information.

      So I'll tell you one and solve the "hard" mystery. I'll define information as the divergence of the distribution of frequencies in a library of molecules from what their distribution would be in an assumed random library. For example, consider all RNA polymers of length 5. There would be 4^5 = 1024 of them. If there were all exhaustively synthesized by some random process, any library with more than 1024 of them would have at least one instance of all possibilities. In a random library, let's say their propensities were each

      fi = 1/1024 for i = 1... 1024

      For all possible sequences, they're equiprobable (this is a big assumption, perhaps organic chemistry might favor some over others.)

      Now let's suppose that you have another, NON-random distribution (library) where their propensities Fi are very different. For example:

      F1 = 1/3
      F5 = 1/3
      F9 = 1/3
      Fi = 0 for all i from 1 to 1024 excluding 1,5 and 9.

      Got that? Non-random distribution. Let's next assume that sequences 1, 5 and 9 had function and all the other i's didn't have function, then this non-random distribution has functional information by Szostak's metric. More specifically I would plug Szostak's metric into Shannon's equation for mutual information.

      (This means that the "divergence from randomness" I speak of would be a Kullback-Liebler divergence of the distribution F1,F2... F1024 from the random distribution f1,f2...f1024.)

      OK so where does the information come from? Suppose that out of those 1024 possible sequences, three (or so) of them could self-replicate.

      Step 1. A natural process could synthesize > 1024 random polymers and it would exhaustively search all possible sequences. The sequences capable of self-replicating would be in the random library. However, the library as a whole would INITIALLY have no information because all propensites would be equal, matching our assumed random background.

      Step 2. The three (or so) sequences that can self-replicate would self-replicate, so then there would be 6 out of 1024, then 12 out of 1024, then 24 out of 1024.. each generation pushes the ACTUAL distribution farther from the random distribution, until non-functional sequences are extinct. This is called Natural Selection and it creates information, assuming self-replicating entities exist. The final distribution would have tons of information, as measured by divergence from randomness.

      That's all. There is no mystery. If self-replicating molecules can be found as a combinatorial possibility within polymers of a certain length, and if abiotic processes can exhaustively search all possible polymers of that length, then natural selection would take over. Natural selection creates information. That is all.

      If you don't like my metric for information, then copy and paste an equation for a better metric. (You won't.)

      Delete
    2. Diogenes wrote:

      "Note there is no definition of "information" in this passage. Creationists never give us an equation for measuring information."

      That has been covered ad nauseum. Its your fault if you have not made your inquiry.

      Complex Specified/instructed Information – It’s not that hard to understand

      Specification or Instruction is a subjective measure. Most people intuitively recognize it and draw conclusions from it. Imagine a deck of cards and a conclusion that just about any reasonable person, with or without knowing what specified/instructed complexity is, will recognize and draw the same conclusion based on it. Then I’ll present a like example from a living thing and ask you be the judge of whether there is specification/instruction.

      Start with a standard deck of 52 playing cards. You are told that it has been shuffled thoroughly. Upon examination you find that the deck is perfectly ordered by suit and rank. Will you still believe it was shuffled? Probably not. Do you know you’ve based that conclusion on specified/instructed complexity? Probably not. Our brains are pattern recognition engines. You reach the conclusion intuitively.

      Let’s dissect this with a bit of arithmetic. Any arrangement of 52 cards is as statistically likely as any other. A random shuffle has no preferred order as an outcome. One arrangement is just as likely as any other. My windows calculator says there are 8.0658175170943878571660636856404e+67 possible arrangements. That’s 8 followed by 67 zeroes and is calculated by entering 52 and then pressing the n! button which performs the calculation 52x51x50x49x48…x5x4x3x2. That is the complexity part – the number of possible arrangments is huge and there is no physical law that prefers one arrangement over another. Most people intuitively know the number of possible arrangements is a huge number without knowing precisely how huge.

      If any one arrangement is as likely as any other why do we conclude the deck was not shuffled if we find it perfectly ordered by rank and suit? Because we intuitively employ the concept of specified/instructed complexity. The perfect ordering is a specification/instruction . Specification/Instruction can be defined as an independently given pattern.

      The problem with this is that specification/instruction is subjective. It is not a product of nature but rather a product of mind. We can’t, or at least I believe we can’t, come up with an objective formula that distinguishes specification/instructions from non-specification/non-instruction. But that doesn’t negate the fact that specification/instruction is tangible and can be practically employed to discriminate between chance and design as we can see with the deck of cards example above.

      Now let us look at an example of specified/instructed complexity that exists in all living things. Lets see a topoisomerase. The enzyme is far more complex than a deck of cards. It is a sequence of hundreds of amino acids in a folded chain. Any link in the chain can be any one of 20 different amino acids. The order determines how it will fold and what biological activity (if any) it will possess. Was it required to specify/instruct to get the amino acid sequence to make if functional specification?

      Delete
    3. Diogenes wrote:

      "This is called Natural Selection and it creates information, assuming self-replicating entities exist."

      my BS detector is on.

      G. F. Joyce, L. E. Orgel, "Prospects for Understanding the Origin of the RNA World," In the RNA World, Cold Spring Harbor Laboratory Press, New York, 1993, p. 13.

      This discussion… has, in a sense, focused on a straw man: the myth of a self-replicating RNA molecule that arose de novo from a soup of random polynucleotides. Not only is such a notion unrealistic in light of our current understanding of prebiotic chemistry, but it would strain the credulity of even an optimist's view of RNA's catalytic potential
      Even if we suppose that there was self-replicating RNA in the primordial world, that numerous amino acids of every type ready to be used by RNA were available, and that all of these impossibilities somehow took place, the situation still does not lead to the formation of even one single protein. For RNA only includes information concerning the structure of proteins. Amino acids, on the other hand, are raw materials. Nevertheless, there is no mechanism for the production of proteins. To consider the existence of RNA sufficient for protein production is as nonsensical as expecting a car to assemble itself by simply throwing the blueprint onto a heap of parts piled up on top of each other. A blueprint cannot produce a car all by itself without a factory and workers to assemble the parts according to the instructions contained in the blueprint; in the same way, the blueprint contained in RNA cannot produce proteins by itself without the cooperation of other cellular components which follow the instructions contained in the RNA.

      The problem of the origin of the RNA World is far from being solved. One can sketch out a logical order of events, beginning with prebiotic chemistry and ending with DNA/protein-based life. However, it must be said that the details of this process remain obscure and are not likely to be known in the near future.

      Delete
    4. The problem with Dembski's argument is that he fails to take into account natural selection, which can account for the "specified complex information" in a topoisomerase. This refutes his claim that CSI can, by itself, be taken as evidence of "intelligent design."

      Delete
    5. Lutesuite

      topoisomerase enzymes are required for dna replication. So you cant explain their origin through evolution.

      Delete
    6. topoisomerase enzymes are required for dna replication.

      No they aren't!

      So you cant explain their origin through evolution.

      Yes you can!

      Delete
    7. How do u know they are not required ?

      Delete
    8. How do u know they are not required ?

      Delete
    9. How do u know they are not required ?

      Education and good careful hard work, to a degree obviously inconceivable to you.

      Delete
    10. ElShamah777 ... who are you? I thought I was talking to Otangelo Grasso ... ;) anyway, here's a question: can a DNA polymerase work without adding a topoisomerase to the reaction mixture? The answer, to save you looking it up, is yes. Yes, I know that's in vitro, but it is a perfectly valid PoC.

      Delete
    11. ElShamah777 ... who are you? I thought I was talking to Otangelo Grasso...

      Not that it matters. With apologies to Yogi Berra: Most of the things Otangelo writes, he didn't actually write.

      Delete
    12. @lutesuite - that's true! He and ElShamah should have a chat. I'm sure they'd discover a shared taste in socks.

      Delete
    13. Ugh what a mess. Grasso cites a paper by Joyce and Orgel that's 23 years old as proof of what's impossible now. Even since 2008 or so there have been a lot of discoveries of processes previously claimed impossible.

      Now that Grasso has given up on his "endoplasmic reticulum is necessary to synthesize a membrane", he now tries a new tack,

      "topoisomerase enzymes are required for dna replication"

      And this will go the same way as his other 'chicken and egg' arguments: no, topoisomerases are NOT necessary to replicate nucleotide polymers. We're talking about RNA here, and they're not needed to replicate RNA.

      For example, viroids, which are circles of RNA. From wikipedia: "Viroid's replication mechanism uses RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid's RNA as a template. Some viroids are ribozymes, having catalytic properties which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[7]

      With Diener’s 1989 hypothesis[8] that viroids may represent "living relics" from the widely assumed, ancient, and non-cellular RNA world—extant before the evolution of DNA or proteins—viroids have assumed significance beyond plant pathology to evolutionary science, by representing the most plausible RNAs capable of performing crucial steps in abiogenesis, the evolution of life from inanimate matter."

      Delete
    14. And further to Grasso's "topoisomerase enzymes are required for dna replication", there's this:

      "In-ice evolution of RNA polymerase ribozyme activity.” James Attwater, Aniela Wochner & Philipp Holliger. Nature Chemistry 5, 1011–1018 (2013). 20 October 2013.
      Abstract: Mechanisms of molecular self-replication have the potential to shed light on the origins of life. In particular, self-replication through RNA-catalysed templated RNA synthesis is thought to have supported a primordial ‘RNA world’. However, existing polymerase ribozymes lack the capacity to synthesize RNAs approaching their own size. Here, we report the in vitro evolution of such catalysts directly in the RNA-stabilizing medium of water ice, which yielded RNA polymerase ribozymes specifically adapted to sub-zero temperatures and able to synthesize RNA in ices at temperatures as low as −19 °C. The combination of cold-adaptive mutations with a previously described 5′ extension operating at ambient temperatures enabled the design of a first polymerase ribozyme capable of catalysing the accurate synthesis of an RNA sequence longer than itself (adding up to 206 nucleotides), an important stepping stone towards RNA self-replication.

      Delete
    15. As for the origin of information, I predicted above that Grasso would not copy and paste in an equation for measuring information. And he didn't.

      Nor did he respond to or address my outline for how information can come about early in the origin of life, so my point about the origin of biological information appears unassailable.

      Instead, Grasso gives a hand-waving summary of ID creationist allegations about information theory, assuming that I haven't heard of them: "That has been covered ad nauseum. Its your fault if you have not made your inquiry."

      Oops! I know more about ID creationist "information" claims that any of the IDers. Grasso's hand-waving description of the features of Dembski's "complex specified information" (CSI) follows Dembski's earlier version in his book No Free Lunch, 2002. Three years later, Dembski significantly redefined CSI in a short paper called "Specification: The Pattern That Signifies Intelligence."

      Since Grasso cites the 2002-and-before version of CSI, I'll refute that version.

      Dembski's < 2002 version of CSI has two components, first, deciding if a sequence or structure is "specified or not" (pre-2005 that was either/or, a yes or no property) and then computing its "complexity" which was here measured as the improbability of the sequence being assembled by randomly scrambling all parts, which I call the "tornado probability."

      Note that the tornado-assembly probabilty is far, far off from the probability of any evolutionary process. To compute it, suppose you have a genetic sequence assembled from a library of A kinds of letters (A= 4 for DNA, or 20 for proteins). If the sequence has a length 2, then the tornado probability of a random sequence is 1/A^2, for a length of 3 it's 1/A^3, and for length L, tornado probabilty is 1/A^L.

      Then Dembksi takes the minus log of the tornado probability, -log(1/A^L), so that's L*log(A). Note that log(A) is a constant, and for DNA or RNA, A= 4 = 2^2, so if you use log base 2, log2(4) = log2(2^2) = 2.

      Thus Dembski's tornado probablity for DNA or RNA is just 2 times the length of the sequence.

      Oops, you can see where this is going. What if there's gene duplication (which happens all the time) and the new genetic sequence is twice as long? L is doubled, so Dembski's CSI is doubled (increased) by known natural processes. This assumes the final sequence is just as specified as the original sequence, which would be the case if the final sequence has a biological function.

      In other words, we know that natural processes create Dembski's CSI, so there's no mystery where it came from.

      For a real world example, consider Lenski's long term evolution experiment. E. coli gained a new function, citrate digestion, through the duplication of some DNA including coding and non-coding functional elements. The new, longer genome had a new function. That's evolution creating an increase in CSI, which falsifies Dembski's claim that only intelligent beings can create CSI.

      Delete
    16. I signed in with another account, ElShamah777 is me.

      Alan Miller wrote

      "Yes, I know that's in vitro, but it is a perfectly valid PoC."

      No, its not. You do not have in vitro conditions in a prebiotic environment.

      Its fascinating to observe how Topoisomerase II enzymes unwind the two strands of the double helix during dna replication to expose the single strands to the enzymes responsible for copying them. Three kind of proteins are absolutely essential in the unwinding process: DNA helicases, topoisomerases, and single-stranded DNA binding proteins (SSB proteins). If one of them is missing, the procedure cannot happen. And here is the interesting part: Instructed information stored in DNA is required to make topoisomerase proteins. Topoisomerase proteins are however required to help unwind the dna strands in order to pass on the genes to code for topoisomerase. The mechanical aspect how they do it is absolutely fascinating and beautyful, a engineering marvel; topoisomerases are able to cut and rejoin small sections of DNA, which require that precise biochemical processes ensure that the right pieces are linked back together and at the right velocity. Too slow, and DNA doesnt unwind fast enough for cell division (mitosis) and the cell dies before replication can occur. Too fast, and it causes irreversible damage and cancer. At minute one, this video shows the process:

      https://www.youtube.com/watch?v=EYGrElVyHnU

      Furthermore, the structure of type IIA topoisomerases requires several key motifs that are indispensable for propoer function:

      N-terminal GHKL ATPase domain

      Toprim domain

      central DNA-binding core

      C-terminal domain

      Each of these key motifs are essential for the proper function of the enzyme. No part can be reduced, and neither is it possible any of the subparts to emerge by natural means. Not only had the enzyme to emerge prior to the first cell being formed, and so could not be the result of evolution, but the sub parts by themself, and the enzyme by itself even fully formed, would have no use, unless the DNA double helix molecules were already existing as well, and so the whole process of cell division, mitosis, and catenation, which happens through DNA replication. The enzyme is however essential for life, so if Topo II is removed, life could not exist. So we have here one of inumerous essential seemingly tiny and aparently unimportant parts, which by closer looking reveal to be life essential. This provides another big question mark in regard of naturalistic explanations, provides on the other part once more a powerful argument for design.

      Delete

    17. No, its not. You do not have in vitro conditions in a prebiotic environment.

      Is it because of the lack of an actual test tube? FFS ...

      Delete
    18. Do you think cancer would have been a problem for early life?

      Delete
    19. Why not? Do you think there were no deseases in early life?

      Delete
    20. Grasso doesn't respond to the debunking of his previous 'chicken and egg' arguments, his claims that a membrane can't be synthesized without the ER, or topoisomerase is necessary for DNA replication therefore no evolution, etc.

      So it's off to a new 'chicken and egg': "the enzyme by itself even fully formed, would have no use, unless the DNA double helix molecules were already existing as well".

      Well, you just assumed that and you assumed wrong. As I already pointed out, at least one of those enzymes, DNA polymerase, has another function: replicating viroid RNA.

      Out of trillions of possible biochemical functions for these molecules, Grasso's proof that 'no other functions are possible' is that he hasn't investigated the subject.

      Delete
    21. Why not? Do you think there were no deseases in early life?

      I don't think cancer was one of them. Think about it.

      Delete
    22. Hee hee. You're a laugh riot, Otangelo.

      Delete
  13. Diogenes wrote:
    "Why couldn't they have been somewhere else besides the ER in earlier lifeforms?"

    Life forms, in whatever stage they may be, require a cell membrane. And a functional cell membrane requires ALWAYS proteins/enzymes/ internal cell parts to manufacture them. NO EXCEPTION.

    ReplyDelete
    Replies
    1. OK, so Grasso has totally ditched his previous argument about how you need an ER to synthesize a membrane. So it's an attempt at goalpost shifting. Rather than admit his first 'chicken and egg' argument was wrong, he's off to just repeating and repeating a different 'chicken and egg.'

      Let's review what Grasso wrote.

      Grasso first said: "The cell membrane is however sinthesized in the ENDOPLASMIC RETICULUM." Caps in the original.

      It was pointed out that bacteria synthesize cell membranes without an ER.

      Grasso #2: "The active sites of the enzymes for the final stages of lipid biosynthesis in endoplasmic reticulum are all found on the cytoplasmic face of the endoplasmic reticulum (and in E. coli, on the cytoplasmic face of the cytoplasmic (inner) membrane. ... So , the cytoplasm, and the mentioned molecules and enzymes are required. They cannot exist without the cell membrane."

      So that didn't fly, so now it's off to

      Grasso #3: "Life forms, in whatever stage they may be, require a cell membrane."

      And it's bye-bye ER. OK, he appears to silently bury that blunder.

      There is certainly no reason to believe that self-replicating information-carrying molecules require a membrane that is synthesized by proteinaceous enzymes (yeah I know this phrase is redundant.)

      Lipids can be synthesized abiotically. They'd be a lot simpler than biosynthesized enzymes, but so what? At early stages in the OOL, the information carrying molecules would be simpler too. They would co-evolve.

      I return to my analogy of trucks and roads. "Road can't be built without trucks, but trucks can't drive unless they're on roads. Therefore, trucks and roads must have come into existence at the same moment!" This is nonsense. Before there were trucks there could be simpler things with the same function, like horse-drawn wagons, and before that, human laborers.

      Before there were asphalt roads there could be simpler roads with a similar function-- brick roads, cobblestone roads (some still in my neighborhood), dirt roads, and animal paths.

      Fun fact: Wilshire Blvd. in Los Angeles today is all paved with asphalt carred in by trucks that need to drive on asphalt. But long ago it was a Native American trail, and long before the Native Americans it was used by woolly mammoths. The mammoths needed no asphalt and no trucks.

      Trucks and roads co-evolved from simpler forms. Likewise, membranes and information-carrying molecules would co-evolve from simpler forms. They did not have to appear simultaneously.

      Delete
  14. Diogenes

    In the article The origin of life we read:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926753/#A002212C436

    Modern cell membranes are composed of complex mixtures of amphiphilic molecules such as phospholipids, sterols, and many other lipids as well as diverse proteins that perform transport and enzymatic functions. Phospholipid membranes are stable under a wide range of temperature, pH, and salt concentration conditions. Such membranes are extremely good permeability barriers, so that modern cells have complete control over the uptake of nutrients and the export of wastes through the specialized channel, pump and pore proteins embedded in their membranes. A great deal of complex biochemical machinery is also required to mediate the growth and division of the cell membrane during the cell cycle.
    Fatty acids are attractive as the fundamental building block of prebiotic membranes in that they are chemically simpler than phospholipids.

    And in the paper : "Membrane Transport in Primitive Cells" they propose monoacyl lipids rather than contemporary diacyl lipids as simpler precursors.

    Whatever membrane you propose, it must be permeable.

    And here come the baseless, speculative just so assertions so common in OOL research papers :
    "Growing multilamellar vesicles with semipermeable membranes would then proceed through a series of shape changes resulting from surface area-volume imbalances and ultimately divide under mild agitation."

    Under mild agitation ? Are they serious ? That sounds just ridiculous. Cell division is extremely complex, and requires also a multitude of fully functional preprogrammed and strictly controlled steps . Cell division isnt a event that happens through " mild agitation". The imagination of the author of the paper is remarkable to say the least.

    ReplyDelete
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    1. That sounds just ridiculous.

      And there, ladies and gentlemen, we have the entire basis of Mr. Grasso's counterargument. The many thousands of published papers each year are failing to take due account of the fact that the research they report sounds ridiculous to Mr. Grasso.

      Delete
    2. There are a lot of papers on abiotic synthesis of lipids and membranes. Grasso has proved this IMPOSSIBLE by finding one article with one sentence he finds implausible...

      ... because Grasso can't believe molecules would be agitated in the ocean. Near, say, a hydrothermal vent. Where superheated liquids are squirting out. And convection currents would make things swirl around in circles. Nah, no agitation there!

      Of course Grasso could just watch any of the many nature documentaries with footage of hydrothermal vents and watch how the hot water is shimmering and swirling and pushing life forms around. But nah. Just say "baseless, speculative just so assertions so common in OOL research papers" and you're done.

      Delete
    3. Judmarc wrote :

      "The many thousands of published papers each year are failing to take due account of the fact that the research they report sounds ridiculous to Mr. Grasso.".

      Thats actually quite right. I can distinguish what makes sense, and what does not. And Abiogenesis proposals, ALL of them, make no sense. And there are GOOD reasons for that.

      Lynn Margulis brought it nicely to the point:

      To go from a bacterium to people is less of a step than to go from a mixture of amino acids to a bacterium.


      Following processes and parts are required to keep cells alive, and illustrate mount improbable to get life a first go:

      http://www.regentsprep.org/regents/biology/2011%20Web%20Pages/Cells-%20Cell%20Basics.htm

      Reproduction. Reproduction is essential for the survival of all living things.
      Metabolism. Enzymatic activity allows a cell to respond to changing environmental demands and regulate its metabolic pathways, both of which are essential to cell survival.
      Nutrition. This is closely related to metabolism. Seal up a living organism in a box for long enough and in due course it will cease to function and eventually die. Nutrients are essential for life.
      Complexity. All known forms of life are amazingly complex. Even single-celled organisms such as bacteria are veritable beehives of activity involving millions of components.
      Organization. Maybe it is not complexity per se that is significant, but organized complexity.
      Growth and development. Individual organisms grow and ecosystems tend to spread (if conditions are right).
      Information content. In recent years scientists have stressed the analogy between living organisms and computers. Crucially, the information needed to replicate an organism is passed on in the genes from parent to offspring.
      Hardware/software entanglement. All life of the sort found on Earth stems from a deal struck between two very different classes of molecules: nucleic acids and proteins.
      Permanence and change. A further paradox of life concerns the strange conjunction of permanence and change.
      Sensitivity. All organisms respond to stimuli— though not always to the same stimuli in the same ways.
      Regulation. All organisms have regulatory mechanisms that coordinate internal processes.

      Delete
    4. Diogenes wrote:

      "Of course Grasso could just watch any of the many nature documentaries with footage of hydrothermal vents and watch how the hot water is shimmering and swirling and pushing life forms around."

      Haha. Thats it ? Thats enough to give life a first go ?

      ho ho ho....

      The US National Academy of Sciences explains, “In water, the assembly of nucleosides from component sugars and nucleobases, the assembly of nucleotides from nucleosides and phosphate, and the assembly of oligonucleotides from nucleotides are all thermodynamically uphill in water. Two amino acids do not spontaneously join in water. Rather, the opposite reaction is thermodynamically favored at any plausible concentrations: polypeptide chains spontaneously hydrolyze in water, yielding their constituent amino acids,” (Luskin). Physicist Richard Morris concurs, “… water tends to break chains of amino acids. If any proteins had formed in the ocean 3.5 billion years ago, they would have quickly disintegrated,” (Morris, 167). Additionally, the cytoplasm of living cells contain essential minerals of potassium, zinc, manganese and phosphate ions. If cells manifested naturally, these minerals would need to be present nearby. But marine environments do not have widespread concentrations of these minerals (Switek). Thus, it is clear, life could not have formed in the ocean.

      Submarine hydrothermal systems (SHSs) have been thought of as a suitable environment for the origin of life subsequent to the abiotic synthesis of organic molecules. However, it has been pointed out that bioorganic molecules, such as amino acids, are easily degraded at a high temperature, and thus not likely to survive for the next step of chemical evolution in a SHS environment.

      The problem with monomers is bad enough,but it is worse with polymers,e.g.,RNA and DNA (Lindahl1993),whose stability in the absence of efficient repair enzymes is too low to maintain genetic integrity iyperthermophiles. RNA and DNA are clearly too unstable to exist in a hot prebiotic environment.The existence of an RNA world with ribose appears to be incompatible with the idea of a hot origin of life.

      Delete
    5. I can distinguish what makes sense, and what does not.

      You can say what makes sense *to you*, on the basis of your vast - or rather, half-vast (say it quickly) knowledge. This has utterly nothing to do with what occurs in reality.

      Delete
    6. Grasso: "the cytoplasm of living cells contain essential minerals of potassium, zinc, manganese and phosphate ions. If cells manifested naturally, these minerals would need to be present nearby. But marine environments do not have widespread concentrations of these minerals (Switek). Thus, it is clear, life could not have formed in the ocean."

      The second sentence is a complete non sequitur. When someone says "It is clear" or "The truth is", it means they don't have evidence.

      Hydrothermal vents contain a wide diversity of iron-sulfur clusters, which are excellent at catalzying a wide diversity of reactions. Moreover, genomic comparisons across the entire tree of life show that some of the oldest sequences are motifs that bind catalytic iron-sulfur clusters, which appear to be the primordial enhancers of abiotic catalysts.

      Delete
    7. Diogenes wrote :

      "Hydrothermal vents contain a wide diversity of iron-sulfur clusters, which are excellent at catalzying a wide diversity of reactions".

      Ahm...kkk

      So these clusters were readily available at hydrothermal vents, nontheless biochemical processes "invented" extremely complex biosynthetic manufacturing processes to synthesize them ? Why is that ?

      ISC system FeS cluster assembly, IscU scaffold (IPR011339)
      http://www.ebi.ac.uk/interpro/entry/IPR011339

      In order to get these, 19 protein complexes are required, which makes this one of the many irreducibly complex biosynthesis pathways :

      An Fe/S cluster is assembled de novo on the scaffold protein Isu1 . Following protein complexes are required:

      1. Cysteine desulfurase complex comprised of Nfs1 and Isd11 Fe/S cluster assembly on Isu1 critically depends on the function of it
      2. Yfh1 (also termed frataxin) functions as an iron donor by undergoing an iron-stimulated interaction with Isu1-Nfs1.
      3. Proteins Mrs3 and Mrs4 Iron is imported into the mitochondrial matrix in its reduced form (Fe2+).This step requires a membrane potential and requires proteins Mrs3 and Mrs4
      4. [2Fe-2S] ferredoxin Yah1 Fe/S cluster assembly on Isu1 further depends on the electron transfer from the [2Fe-2S] ferredoxin Yah1
      5. Specific amino acid ligands assembly into the apoprotein by coordination with the specific amino acid ligands.
      6. Ssq1
      7. Jac1
      8. Mge1 its transfer to apoproteins and its assembly into the apoprotein by coordination with the specific amino acid ligands. This step is specifically assisted by a dedicated chaperone system comprised of the Hsp70 family member Ssq1, the DnaJ-like co-chaperone Jac1 and the nucleotide exchange factor Mge1
      9. Monothiol glutaredoxin Grx5 Another important function in this partial reaction is performed by the mitochondrial monothiol glutaredoxin Grx5, yet its precise role is unknown hitherto.
      10.ISC assembly machinery Apparently, the function of this machinery is critical for the ability of the cell to generate extra-mitochondrial Fe/S proteins,
      11. ABC transporter Atm1 The export reaction is accomplished by the ABC transporter Atm1
      12. Sulfhydryl oxidase Erv1
      13. Glutathione (GSH) The sulfhydryl oxidase Erv1 of the intermembrane space and glutathione (GSH) are required.
      14. Cytosolic iron-sulfur protein assembly (CIA) system Maturation of the cytosolic and nuclear Fe/S proteins is catalyzed by the cytosolic iron-sulfur protein assembly (CIA) system comprised of five known proteins
      15. Ploop NTPases Cfd1 and Nbp35 An Fe/S cluster is transiently assembled on the Ploop NTPases Cfd1 and Nbp35 which serve as a scaffold.
      16. Mitochondria. Ploop NTPases Cfd1 and Nbp35 which serve as a scaffold. This step essentially requires mitochondria.
      17. CIA proteins Nar1, Cia1 and Cia2 Cfd1 and Nbp35 involved in activation of CIA protein Nar1 by assembly of two Fe/S clusters on this iron-only hydrogenase-like protein

      Essential Fe/S proteins:

      1. Essential cytosolic-nuclear Fe/S protein is Rli1 a component involved in ribosome assembly and export from the nucleus
      2. Two other essential (nuclear) Fe/S proteins with a function in nucleotide excision repair (Rad3) and RNA primer synthesis for DNA replication (Pri2)

      Delete
  15. Gary Gaulin wrote at his blog :

    "Surface volcanic eruptions would be producing intense lightning storms that create among other things amino acids"

    Gary, could you point out in detail how that happened ? The production of amino acids in cells require a multitude of complex biosinthetic processes. Why did cells emerge with these pathways, if amino acids were supposedly readily available through volcano eruptions ? And did these eruptions transform nitrogen miraculously into useful fixed form ? How did the sorting out of 20 amino acids out of over 500 existing happen ? And how did prebiotic chemistry sort out wich were left handed, and selecting them out ?

    Gary wrote :

    "Wetting and drying cycles would then polymerize the amino acids into proteins to (when wet) form a protein plasma similar to what is inside of cells."

    Amazing.

    Bruce Alberts admits :

    we can walk and we can talk because the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered. Proteins make up most of the dry mass of a cell. But instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules. And, as it carries out its biological functions, each of these protein assemblies interacts with several other large complexes of proteins. Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines. […]

    If there would exist a degree and post doctorate for pseudo science, you could certainly apply to get it with ease. Congrats.



    ReplyDelete
  16. Whew, astounding! "Bible" Byers, "Cut 'n' Paste" Grasso , Gary "The Programmer" and whatever a Cruglers is all on a single thread. Quick, someone send an Evite to JoeG.

    Seriously, though, this thread represents the level of "science" that would be introduced into US public schools if creationist-leaning state legislatures and school boards had their sway. We've seen these attempts in a number of states but most notably in Kansas, Louisiana, Kentucky, Texas, Pennsylvania and Ohio. All have required intervention by science educators at considerable cost and effort.

    ReplyDelete
  17. Happy this guy will be moving out of the governor's mansion in Indiana. Sorry to hear that some believe America "deserves" Trump and Pence.

    ReplyDelete
  18. "My training is in the law ... " ... Oh, do go on.

    ReplyDelete
  19. The latest from the Ark Park indicates a rapid sinking to "rock bottom" of the cycle:
    https://thenaturalhistorian.com/2016/07/31/ken-hams-ark-encounter-opens-to-a-flood-of-press-but-fewer-visitors-than-anticipated/

    We can expect that the on-average low income taxpayers who are going to be stuck with the bills are going to stop being polite the next time Ken and others talk about needing more money to fight "scientists" and others who are supposedly busy all day conspiring against them in order to destroy religion. Their real problem of course is that too many people know what's actually in the geological formations and it's certainly not a homogeneous mixture of trilobites to humans.

    Denial is catching up to AIG. With Mike Pence being such a visible enabler it could also have a major backlash against the Republican party and Donald Trump's campaign. They are in the same boat together, and could all go down with the ship.

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  20. Let's face it. We are not going to get any experimental evidence for the origins of life!!!

    Why? Because if there was such evidenced, intelligence, though very limited, should have already surpassed the random processes that apparently brought life into existence, should they?

    ReplyDelete
  21. Cruglers, what are you trying to say? The sentence that follows "Why?" doesn't communicate.

    ReplyDelete
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    1. Incoherent sentences don't matter - the three exclamation points after his first sentence trumps everything.

      "Trumps" in the sense of "typical of the so-called thought processes of a certain presidential candidate."

      Delete
    2. He is essentially trying to say that our highly organized intelligence should already understand the origin of life if it arose from dumb random chemistry.

      Obviously there is something numinous (god) about the origin of life that prevents our understanding.

      If he were alive in past centuries, he would be saying the same about volcanoes, tornadoes, and the plague.

      Delete
    3. Since you don't have the good one, (I'm sure of that) just give me the comfort one for the ones who need it to "feel good" about themselves..

      Delete
  22. Diogenes,

    How many pieces of evidence have you accumulated so far that have made up your mind that life originated by accident and that prokaryotic cell has evolved to eukaryotic cell after the miracle?

    Just give me 1 related to the topic experiment link and I will settle down....

    ReplyDelete
    Replies
    1. Cruglers did not address any of my points. He stated there was no evidence for endosymbiosis. I listed a bunch. He seeks to exhaust us through repetition of "There is no evidence" when we shove it under his nose.

      Now we get straw man attack: I have "made up your mind that life originated by accident." No, scientists generally think that non-random structures result from non-random processes. Not "accident". I sketched an outline for Grasso above, Step 1, Step 2, etc. The non-random information is not due to "accident."


      "evolved to eukaryotic after the miracle". Ugh, this is projection. Creationists believe in miracles. We don't. This is the Karl Rove-ian strategy of "Accuse your enemy of your own worst defect." (It got Bush re-elected.)

      And this is dishonest: "Just give me 1 related to the topic experiment link and I will settle down"-- because I listed a bunch, and the Hatena experiment I cited twice. But he keeps repeating there is no evidence. Argument by exhaustive repetition of Nuh-Uh.

      Delete
    2. Diogenes

      1. Why are there cases where eukaryotic mitochondria have linear genomes with eukaryotic telomeres ?
      2. The translocon of the outer-chloroplast-envelope subunit TOC75 to bacterial outer-membrane proteins that are involved in the transport of polypeptides across the outer membrane of Gram-negative bacteria, so they are homologues. What however about the translocon of the inner chloroplast envelope (TIC)? There is no detectable homologue for the TIC110 channel, and the second channel subunit TIC20 shows only a low homology to bacterial proteins. The homology is used to infer endosymbiosis. What do you infer imho, when there isnt ? Then its time, as the following paper does :

      file:///E:/Desktop/apdf%20files/protein%20import%20of%20chloroplasts.pdf

      to make things up, and just assert that the subunits were " eukaryotic additions ". Homology can well be explained through common design. Thats common practice. Examples which seem to fit evolutionary assumptions are cited, while the examples that do not fit are ignored, or baseless assertions are made, as the cited paper does. The many similarities that exist among members of the animal kingdom can well be the result of the fact that a single designer created the basic kinds of living 'systems', then specially modified each type of life to enable it to survive in its unique environmental niche.
      3. According to the scientific paper "Did DNA replication evolve twice independently?" several core components of the bacterial replication machinery are unrelated or only distantly related to the functionally equivalent components of the archaeal/eukaryotic replication apparatus.
      4. Ann Gauger points out that There is no single proposed mechanism for the evolution of the nucleus or the other structures I have named. I deliberately call such evolutionary accounts "stories."
      5. Mitochondria in invertebrates use a different genetic code from the mitochondria in vertebrates, and both of those codes are different from the “universal” genetic code, what does that tell us?

      Delete
  23. Diogenes,

    If you'd designed something marvels, something you took pride in ( let's say it was the highest building in the world) and after a while you've found out that someone else took credit for your design, how would you feel about it? How would you feel if the project of your design was attributed to someone else?

    Can you feel it?

    What would you do about it?

    Would you let it go?

    ReplyDelete
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    1. If I was your omnipotent, omniscient, invisible and non-existent friend I would not give a shit what the ants on this ball of mud got up to. Except to get out my giant magnifying glass every once in a while. Actually not necessary as the ants on this particular ball of mud seem to busy devising their own magnifying glass.

      I especially would not concern myself with what they get up to whilst naked in the privacy of their own homes.

      Delete