The pathway to this event is complex and requires multiple mutations [see On the unpredictability of evolution and potentiation in Lenski's long-term evolution experiment and Lenski's long-term evolution experiment: the evolution of bacteria that can use citrate as a carbon source].
One of those creationists is Scott Minnich1, a professor and researcher at the University of Idaho in Moscow, Idaho (USA). Minnich wants you to believe that the LTEE isn't significant because no new genetic information was created. This is part of a strategy to accept microevolution but deny that macroevolution can be explained by naturalistic processes.
Minnich's lab did some experiments in order to replay the evolution of citrate utilization in E. coli cultures. They found that they could evolve strains that utilized citrate under aerobic conditions but in their hands it took much less time than it took in the LTEE and it was much more likely to occur. (Recall that the Cit+ phenotype only evolved in one of the twelve cultures in the LTEE and it took 30,000 generations.) Here's the Minnich paper and the abstact.
Van Hofwegen, D.J., Hovde, C.J., and Minnich, S.A. (2016) Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA. Journal of bacteriology, published online Feb. 1, 2016 [doi: 10.1128/JB.00831-15]
ABSTRACY The isolation of aerobic citrate-utilizing Escherichia coli (Cit+) in long term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit+ mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested with wild-type E. coli B, K12, and three K12 derivatives: E. coli ΔrpoS::kan (impaired for stationary phase survival), E. coli ΔcitT::kan (deleted for the anaerobic citrate/succinate antiporter) and E. coli ΔdctA::kan (deleted for the aerobic succinate transporter). E. coli underwent adaptation to aerobic citrate metabolism that was readily and repeatedly achieved using minimal medium supplemented with citrate (M9C), M9C with 0.005% glycerol, or M9C with 0.0025% glucose. Forty-six independent E. coli Cit+ mutants were isolated from all E. coli derivatives except E. coli ΔcitT::kan. Potentiation/actualization mutations occurred within as few as 12 generations and refinement mutations occurred within 100 generations. Citrate utilization was confirmed using Simmons-, Christensen-, and LeMaster Richards citrate media and quantified by mass spectrometry. E. coli Cit+ mutants grew in clumps and long incompletely divided chains, a phenotype that was reversible in rich media. Genomic DNA sequencing of four E. coli Cit+ mutants revealed the required sequence of mutational events leading to a refined Cit+ mutant. These events showed amplified citT and dctA loci followed by DNA rearrangements consistent with promotor capture events for citT. These mutations were equivalent to the amplification and promoter capture CitT-activating mutations identified in the LTEE.
IMPORTANCE E. coli cannot use citrate aerobically. Long term evolution experiments (LTEE) by Lenski found a single aerobic, citrate-utilizing E. coli after 33,000 generations (15 years). This is interpreted as a speciation event. Here we show why it probably is not. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are the same class of mutations identified by the LTEE. We conclude the rarity of the LTEE mutant was an artifact of the experimental conditions, not a unique evolutionary event. No new genetic information (novel gene function) evolved.
Blount and Lenski discuss two technical points: the rapidity of the events in the Van Hofwegan et al. paper and the criticism of historical contingency in that paper and in an accompanying commentary by Roth and Maisnier-Patin (2016). Neither criticism is valid.
(Blount has published a nice paper on historical contingency in the LTEE (Blount, 2016). It's relevant to our discussions about replaying the tape of life.)
Blount and Lenski also address the creation of new genetic information. They say,
The claim that “no new genetic information evolved” is based on the fact that the bacteria gained this new ability by rearranging existing structural and regulatory genetic elements. But that’s like saying a new book—say, Darwin’s Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books.This is an important point.
In an evolutionary context, a genome encodes not just proteins and patterns of expression, but information about the environments where an organism’s ancestors have lived and how to survive and reproduce in those environments by having useful proteins, expressing them under appropriate conditions (but not others), and so on. So when natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria.
That’s how evolution works—it’s not as though new genes and functions somehow appear out of thin air. As the bacterial geneticist and Nobel laureate François Jacob wrote (Science, 1977): “[N]atural selection does not work as an engineer works. It works like a tinkerer—a tinkerer who does not know exactly what he is going to produce but uses whatever he finds around him, whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a tinkerer who uses everything at his disposal to produce some kind of workable object.”
To say there’s no new genetic information when a new function has evolved (or even when an existing function has improved) is a red herring that is promulgated by the opponents of evolutionary science.
Evolution works by modifying pre-existing DNA to create new genes or new regulatory elements from sequences that were already present in the genome.2 Creationists seem to think that new genetic information has to be "poofed" into existence from nothing or it doesn't count as new information. They would like very much to demonstrate that there are real examples of such magic because that would lend support to their claim that goddidit. So far they haven't come up with a single, credible, example of such a gene so they have to be content with denying that evolution can create new genetic information.
It's sad, really.
1. Minnich is a fellow at the Center for Science and Culture (Discovery Institute).
2. There are some exceptions, let's not quibble.
Blount, Z.D. (2016) A case study in evolutionary contingency. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences. [doi: 10.1016/j.shpsc.2015.12.007]
Biological evolution is a fundamentally historical phenomenon in which intertwined stochastic and deterministic processes shape lineages with long, continuous histories that exist in a changing world that has a history of its own. The degree to which these characteristics render evolution historically contingent, and evolutionary outcomes thereby unpredictably sensitive to history has been the subject of considerable debate in recent decades. Microbial evolution experiments have proven among the most fruitful means of empirically investigating the issue of historical contingency in evolution. One such experiment is the Escherichia coli Long-Term Evolution Experiment (LTEE), in which twelve populations founded from the same clone of E. coli have evolved in parallel under identical conditions. Aerobic growth on citrate (Cit+), a novel trait for E. coli, evolved in one of these populations after more than 30,000 generations. Experimental replays of this population's evolution from various points in its history showed that the Cit+ trait was historically contingent upon earlier mutations that potentiated the trait by rendering it mutationally accessible. Here I review this case of evolutionary contingency and discuss what it implies about the importance of historical contingency arising from the core processes of evolution.
Roth, J., and Maisnier-Patin, S. (2016) Re-interpreting long-term evolution experiments—Is delayed adaptation an example of historical contingency or a consequence of intermittent selection? Journal of bacteriology, JB. 00110-00116. [doi: 10.1128/JB.00110-16]
226 comments :
«Oldest ‹Older 201 – 226 of 226No, I'm sorry Brian, but you have no argument. The chemistry that occurs in cells is extremely functional and precisely regulated. This isn't that hard.
Tx:
"No, proteins serve purposes."
Do they now? Like causing allergies and cancer you mean?
"The chemistry that occurs in cells is extremely functional and precisely regulated."
Uh huh, once chemistry goes outside of cells, it all becomes utter chaos... No chemical reaction is ever the same, is it?
So you're saying every chemical reaction attempted outside a cell will never give the same result. Do tell this to forensic investigators before their evidence puts someone on the chair for murder.
A solution of Litmus changes color at random obviously.
No chemical reaction is ever the same, is it?
Honestly, txpiper, if we were trying to make up quotes for you to make you look stupid, we couldn't improve on the stuff you actually write yourself.
The dividing line between chemistry and biochemistry is purpose and function. You could call it mission.
There's a dividing line, eh? OK, then you'll be able to show me your dividing line in how the quantum physics of electron shells (which is where chemistry happens) is different for biochemistry than "normal" chemistry. I'll just wait for your answer.... (Oh, and while I'm waiting, please tell me the "mission" of amino acids that fall to earth from space in meteorites.)
And you have no mechanism to account for their origins or their role. I'll go with the idea that they do what they do because they were designed to do it.
All you have is design because you don't understand the mechanism, which as I noted before has to do fundamentally with the quantum physics of electron shells. But believe me, you don't want to learn about this stuff, because once you understand the chemistry and biochemistry, there goes the personal incredulity your entire belief system is based on.
It's really wonderful (in the older, original sense of the word, something that makes one full of wonder) how the Internet enables fools who think the Earth was poofed into existence in a week 6000 years ago (yourself), or who think bacteria have opinions (Steve) to think they're actually debating science with a university biochemistry professor who literally wrote the book.
@lutesuite, I believe that was Ed characterizing what txpiper thinks, rather than something txpiper said. It certainly is implied by what txpiper said, as Ed correctly pointed out.
txpiper: "No, I'm sorry Brian, but you have no argument."
No, the arguments have been had ad nauseum, round and round in circles in thread after thread. You are just too ignorant of the level of resolution to which physical reality has been elucidated and characterized and blinded by your metaphysical commitments to be receptive to them. Your "arguments" are nothing more than uninformed assertions and statement of incredulity. A hopeless cause, but fortunately a dead end.
Sorry, my mistake.
You all are debating whether an organisms ability to rearrange DNA as a means to lose/gain function points to your philosophical beliefs. Round and round you go with meaningless thought. What a waste of your time! Science cannot prove evolution exists just as science cannot prove God exists.
Science cannot prove evolution exists
Ah, a visitor from the 1840s! :-)
Of course functionally "new" information was evolved in these citrate utilization experiments. It just was just very very low-level functional information that didn't require the evolution of anything structurally new. If all that has to happen in the transfer of one particular "word" or "phrase" in a book to another particular spot in the book for some new functionality to be realized, well, the odds of success are very high indeed. Again, all that happened here is that a pre-formed gene was transferred from one place to another fairly specified place within the genome. That's it. Clearly, that's statistically likely in relatively short order.
But, that's not the real problem for the Darwinian mechanism or for the Theory of Evolution in general. The real challenge is in explaining how random mutations can search through the vastness of protein sequence space (a space comprised of all possible sequences of a particular length) to find the extremely rare islands of novel beneficial sequences that could produce something qualitatively new - an entirely new type of function that requires an new protein-based system - a new physical structure. Such unicorns are much harder to find because random mutations have to search through vast oceans of non-beneficial sequences before they can find the very rare isolated islands of beneficial sequences. The question is, are there any examples of this sort of evolution actually happening?
Well, yes, there are many examples were truly novel protein sequences with selectably beneficial functionality are discovered by random mutations. Most of these examples are single-protein enzymes and the like that require a minimum of no more than a few hundred specifically arranged amino acid residues (amino acids are the building blocks of proteins, with a total of 20 different amino acid "characters" within the "alphabet" of proteins). However, there are no examples of evolution in action producing any protein-based system that requires a minimum of more than 1000 specifically arranged amino acid residues - not even close. The reason for this is because sequence space at this level is unimaginably enormous (i.e., 20^1000 = 1e1301 sequences). To get an idea as to how large this number is, consider that the total number of atoms in the visible universe is about 1e80 atoms. What is more important, however, is that the ratio of potentially beneficial vs. non-beneficial sequences in the 1e1301 sequence space is incredibly tiny - so minuscule that any cluster of beneficial sequences in the enormity of sequence space is surrounded, on all sides, by an enormous ocean of non-beneficial sequences that is so vast that, if the beneficial islands of sequences were like stars in the sky, no other stars would be visible in the universe from the perspective of one of these islands. That means that getting from one of these islands to the next closest beneficial island, by random mutations, would take trillions upon trillions of years of time.
More at: http://www.detectingdesign.com/Lenski.html
Proteins need to interact together. They need interface compatibility. So this adds to the unsurmountable problem ot making them by chance. Lets say our good old friend chance , after 10^78 trial and errors , got a functional protein made. That function has imho no value, if it cannot interact properly with other proteins. Then our same old friend made another 10^78 trial and errors attempts, and got the second protein made. How many attempts would be required to make them compatible to be able to interact in a functional way ? So lets suppose for a moment, that they got the right interface compatibility, and interact properly . So what ? This interaction alone has a long way to go, to get all 20 protein complexes needed to get DNA replication done, and making them interact all together in a functional way. Its the same as to make a piston by trial and error. At the end you have eventually a device that is piston like. If you do not know imho exactly the size the piston has to have to fit into the motor block, nothing done. Nothing will go. So FORSIGHT and INTELLIGENCE in order to PROJECT the whole device is ESSENTIAL.
Sean, your website is a great source of information. Learned a lot there. Thanks for your great work.
Sean Pitman's argument has already been shown to be so much balderdash in the article linked below. Sean doesn't let that faze him. He just marches on, pulling enormous (but meaningless) numbers out his ass, like the good Christian soldier he is. Who needs sound arguments, when you've got Faith?
Probability and Evolution
I'm sure Dr. Pittman appreciates the endorsement of a lying, ignorant, internet troll like yourself, Otangelo. It's about the best he can get.
Read the article by Jason Rosenhouse I linked above. It explains, in clear terms, why the Argument from Rectally Extracted Really, Really Big Numbers, so beloved of IDiots like yourself and Sean Pittman, is a non-sequitur.
Otangelo, if you want an example of something utterly, vanishingly unlikely, it is that you and Sean Pitman have greater expertise in this area than Richard Lenski.
You linked Jason Rosenhouse to explain how to climb "Mt. Improbable"? Really?
While he's a mathematician, he really doesn't understand biological complexity and how potentially beneficial protein-based systems are arranged in sequence space… at various levels of functional complexity. He has this vision of closely-spaced steppingstones lined up in neat little rows across the vastness of the otherwise desolate ocean of sequence space options (at all levels of sequence space regardless of size).
Of course, it would be wonderful if this were the case. The problem, however, is that this view of sequence space simply not a realistic view of reality. In the real world the potentially beneficial targets within sequence space have a fairly uniform distribution across that space. They simply aren’t lined up in neat little rows like Rosenhouse and other evolutionists imagine. And, with each step up the ladder of functional complexity (i.e., with each increase in the minimum size and/or specificity requirements) not only does the size of sequence space increase exponentially (by 20 fold with each step up the ladder), but the ratio of potentially beneficial vs. non-beneficial sequences decreases exponentially as well. And, given their uniform distribution within sequence space, the minimum likely distance between a given steppingstone and the next closest potentially beneficial steppingstone (with a qualitatively novel function) increases in a linear manner. And, what this means is that the average time required to find such a steppingstone increases exponentially. . . which very quickly turns into a very serious problem for the Darwinian mechanism beyond they very lowest rungs of the ladder of functional complexity.
Lenski’s experiments have by no means addressed this problem – not by a long shot. The “new functions” that Lenski produces in his lab are at the very lowest levels of functional complexity. They aren’t based on producing anything structurally new within the genome. They are entirely based on placing a pre-existing gene that is fully functional in a new place within the genome where it will be transcribed under oxic conditions. That’s it. And, that’s very easy to do since it is so statistically likely! – extremely easy in fact! It can be achieved in a handful of generations under the right conditions within a relatively small population of bacteria.
However, when you try to evolve something qualitatively new that wasn’t already in the genome somewhere doing the very same job (except perhaps under different environmental conditions), when you have to come up with a novel protein-based system with new proteins or new specific 3D interactions between even pre-existing proteins in order to produce qualitatively novel functionality, you have a much bigger problem on your hands. Why? Because, statistically speaking, it is much less likely to have pre-existing genes/proteins that don’t require multiple modifications (none of which are sequentially selectable) before the new beneficial function can be realized to any selectable degree of functionality. And, this problem only grows, exponentially, with each increase in the minimum structural requirements of the system in question.
For more on my debate with Rosenhouse in particular see:
http://www.detectingdesign.com/JasonRosenhouse.html
LS
Here is the argument.
"I certainly agree that natural selection has never been observed to produce something as complex as the vertebrate eye. Intelligent agents have never been observed to bring universes into being or to create life from scratch, but Sean has no trouble believing that occurred. The fact remains that there is voluminous circumstantial evidence supporting the claim that natural selection can in principle and has in natural history produced complex adaptations. When you contrast this with the perfect vacuum of evidence supporting the existence of intelligent designers who can do what ID folks say they can do, it becomes clear why scientists are all but unanimous in preferring evolution over intelligent design."
This is what you think shuts down Sean's argument?
You cited Jason Rosenhouse to explain how to climb "Mt. Improbable"? Really? Did you read the rest of the discussion in the comment section of the post? – and how Rosenhouse argues that it’s really all based on “circumstantial evidence” without having to actually understand how the actual mechanism of random mutations and natural selection could have done it beyond the lowest levels of functional complexity?
While Rosenhouse is a mathematician, he really doesn't understand biological complexity and how potentially beneficial protein-based systems are arranged in sequence space . . . at various levels of functional complexity. He has this vision of closely-spaced steppingstones lined up in neat little rows across the vastness of an otherwise desolate ocean of sequence space options.
Of course, it would be wonderful if this were the case. The problem, however, is that this view of sequence space simply not realistic. In the real world the potentially beneficial targets within sequence space have a fairly uniform distribution across that space. They simply aren’t lined up in neat little rows like Rosenhouse and other evolutionists imagine. And, with each step up the ladder of functional complexity (i.e., with each increase in the minimum size and/or specificity requirements) not only does the size of sequence space increase exponentially (by 20 fold with each step up the ladder), but the ratio of potentially beneficial vs. non-beneficial sequences decreases exponentially as well. And, given their uniform distribution within sequence space, the minimum likely distance between a given steppingstone and the next closest potentially beneficial steppingstone with a qualitatively novel function increases in a linear manner. What this means is that the average time required to find such a steppingstone increases exponentially. . . which very quickly turns into a very serious problem for the Darwinian mechanism beyond they very lowest rungs of the ladder of functional complexity.
Lenski’s experiments have by no means addressed this problem – not by a long shot. The “new functions” that Lenski produces in his lab are at the very lowest levels of functional complexity. They aren’t based on producing anything structurally new within the genome. They are entirely based on placing a pre-existing gene that is fully functional in a new place within the genome where it will be transcribed under oxic conditions. That’s it. And, that’s very easy to do since it is so statistically likely! – extremely easy in fact! It can be achieved in a handful of generations under the right conditions within a relatively small population of bacteria.
However, when you try to evolve something qualitatively new that wasn’t already in the genome somewhere doing the very same job (except perhaps under different environmental conditions), when you have to come up with a novel protein-based system with new proteins or new specific 3D interactions between even pre-existing proteins in order to produce qualitatively novel functionality, you have a much bigger problem on your hands. Why? Because, statistically speaking, it is much less likely to have pre-existing genes/proteins that don’t require multiple modifications (none of which are sequentially selectable) before the new beneficial function can be realized to any selectable degree of functionality. And, this problem only grows, exponentially, with each increase in the minimum structural requirements of the system in question.
For more on my debate with Rosenhouse in particular see: Link
To get from one protein function to the next, usually not one, but several mutations need to occur, and and a new line up of amino acids that confer a new function of the protein.
I posted at the topic Irreducible complexity is a undeniable fact, at my library:
When Lenski et al. created a simulation with high irreducible complexity, i.e. there was no selective advantage until the target function arose, EQU never evolved! Consider this quote from the Lenski paper:
"At the other extreme, 50 populations evolved in an environment where only EQU was rewarded, and no simpler function yielded energy. We expected that EQU would evolve much less often because selection would not preserve the simpler functions that provide foundations to build more complex features. Indeed, none of these populations evolved EQU, a highly significant difference from the fraction that did so in the reward-all environment (P ~= 4.3 x 10-9, Fisher's exact test)."
In other words, when there is no selective advantage until you get the final function, the final function doesn't evolve.
Meyer writes:
What natural selection lacks, intelligent design—purposive, goal-directed selection—provides. Rational agents can arrange both matter and symbols with distant goals in mind. In using language, the human mind routinely "finds" or generates highly improbable linguistic sequences to convey an intended or preconceived idea. In the process of thought, functional objectives precede and constrain the selection of words, sounds, and symbols to generate functional (and meaningful) sequences from a vast ensemble of meaningless alternative possible combinations of sound or symbol. Similarly, the construction of complex technological objects and products, such as bridges, circuit boards, engines, and software, results from the application of goal-directed constraints. Indeed, in all functionally integrated complex systems where the cause is known by experience or observation, designing engineers or other intelligent agents applied constraints on the possible arrangements of matter to limit possibilities in order to produce improbable forms, sequences, or structures. Rational agents have repeatedly demonstrated the capacity to constrain possible outcomes to actualize improbable but initially unrealized future functions. Repeated experience affirms that intelligent agents (minds) uniquely possess such causal powers. Analysis of the problem of the origin of biological information, therefore, exposes a deficiency in the causal powers of natural selection and other undirected evolutionary mechanisms that corresponds precisely to powers that agents are uniquely known to possess. Intelligent agents have foresight. Such agents can determine or select functional goals before they are physically instantiated. They can devise or select material means to accomplish those ends from among an array of possibilities. They can then actualize those goals in accord with a preconceived design plan or set of functional requirements.
@ Sean Pittman:
It's always a bit astonishing to be reminded of how little creationists understand evolutionary theory, despite the inordinate amount of time they devote to trying to refute it. Many of the misconceptions in your post are directly addressed in Larry Moran's article above, as well as in Jason Rosenhouse's post. In brief:
- The type of "new functions" you are looking for do not occur in nature. All novelty results from modification of pre-existing functions and structures. This is what would be predicted from evolutionary theory. Ironically, the type of "new functions" you demand are what would occur if intelligent design/creationism were true. We don't see them. What should be concluded from this?
- Evolution does not proceed solely thru a series of beneficial mutations. By far the greater proportion of evolutionary change occurs thru neutral or slightly deleterious mutations. This is what bridges the transitions between beneficial "stepping stones" that so perplex you. Also, the fitness landscape is not static, but constantly changes with the environment. IOW, your assessment of whether a particular sequence is functional or beneficial is entirely based on wild guesses. You have no way of knowing which pathways thru sequence space may have been available in the remote past.
- Evolution does not work towards pre-determined conclusions. So the improbability of any particular functional sequence arising is irrelevant. To illustrate: On March 2, 2016, a man named James Stocklas won $291.4 million in the Florida Powerball lottery, with the winning numbers 12, 12, 44, 52, 62 and 6. Can you appreciate how massively improbable this was? To begin with, the odds for anyone who buys a ticket of winning the draw are only 1 in 292,201,338. But, beyond that, there are so many other factors that had to line up just right for this to happen. The number 53 could have been drawn instead of 52. The jack pot could have been only $291.3 million. The draw could have occurred on March 9 rather than March 2. James Stocklas might not have purchased a ticket that week. Mr and Mrs Stocklas could have named their son George instead of James. A giant meteor could have hit the earth 4 billion years ago and obliterated it. Etc. So, as you can see, the odds of this specific event occurring are so low that it would have been virtually impossible to have predicted it in advance. And, yet, it happened. So does that mean James Stocklas's winning the lottery proves the existence of God? Or does it mean, instead, that you do not understand probability theory as it applies to evolution? I know where I would place the odds.
@ Otangelo Grasso
This is what you think shuts down Sean's argument?
What shuts it down is that it is based on fallacious arguments based on false premises and an inadequate understanding of basic evolutionary theory. That's all.
It's almost sad how desperately Sean craves the approval of actual scientists like Richard Lenski, and all he gets is the admiration of imbecilic religious zealots like Otangelo Grasso.
Hey Sean, this problem has been solved before, here's recent study: http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003818
The problem is you imagine something like only point mutations must accumulate and slowly build a new protein from scratch. If that was the only source of mutation available to evolution you'd be right, structurally new proteins would take extremely long time to evolve.
Problem for you is, that's not the only type of mutation possible. New proteins can be produced by the accretion and/or fusion and recombination of fragments of other proteins. So instead of having to generate, say, significant stretches of amino acids one at a time, through the incremental accumulation of mutations until you end up with a beta-sheet or alpha helix, what can instead happen is fragments of already existing proteins are recombined to produce new structures. As the paper I linked shows, once such types of mutations are included (duplications, inversions, insertions, fusions and so on, all of which are observed types of mutations), the generating "new" proteins is well within the capability of the evolutionary process.
Or alternatively, previously non-coding regions can mutate such that they become transcribed and translated, and by chance this new region that previously was not coding, once translated, produces a new functional protein of some sort. There is phylogenetic evidence that things like this have happened for some ORFan protein coding genes.
@Pitman: "The problem, however, is that this view of sequence space simply not realistic. In the real world the potentially beneficial targets within sequence space have a fairly uniform distribution across that space."
Flat out made up shit, Sean. You have no idea what functions exist in unprobed areas of sequence space. The only thing you can show is that functions that are currently used by life are not all found close to each other. But you cannot extrapolate from this to show that there are no other functions out there, or that one function can't be reached from another. Or that a high catalytic rate of an enzyme, or a very strong and specific binding pocket, can't be evolved through cumulative selection from a more broadly catalytic pocket with lower kinetics. In fact, we have evidence that it is usually the case that we CAN reach highly specific functions and strong binding energies from more promiscous or weaker ancestral stages that exist at much, much higher frequencies.
All you can show is that, from what we know of proteins used in life that currently exists, there's one function here, and another over there. What lies between them you have no idea of, you have to test for that. Actaully, what we know of physics and enzyme chemistry tells us that there's probably always some low level of function nearby that can be improved with cumulative selection. It seems to follow from the basic physics of organic polymers, and it is time and time again borne out by actual experiments that try to probe the functionality of sequence space for novel functions, even using totally random sequences unrelated to anything found in life.
"They simply aren’t lined up in neat little rows like Rosenhouse and other evolutionists imagine."
Actually it is you who imagine that the functions are isolated by vast seas of nonfunctionality, yet you have no evidence in support of this. All you have is what functions are known to exist, you don't have any data from unprobed areas, and you can't extrapolate from the known into the unknown areas.
"And, with each step up the ladder of functional complexity (i.e., with each increase in the minimum size and/or specificity requirements)"
You can't speak of both size and specificity as if they go hand in hand in this way. In fact we know of cases where it does not. Once a function is found, decades of experiments in artificial selection has shown that (for example) enzyme substrate specificity and catalytic rate can be massively narrowed down, and increased(respectively) without increasing the size of the protein (or Ribozyme).
Now, it is true that the more specific the function (again using enzymes as an example, substrate specificity narrowed to a single substrate) the less space it takes up in sequence space, but that's irrelevant, since the evolutioanarily relevant question is if some some degree of function even if quite weak and unspecific, can be reached from an arbitrary location and then whether the more specific function can be reached by incremental selection from there. All experiments done to date show that this is the case. That it takes relatively few mutations from an arbitrary location in sequence space, to find something at least weakly functional, and that subsequent to this, functional specificity can be massively increased from there through cumulative selection.
"not only does the size of sequence space increase exponentially (by 20 fold with each step up the ladder), but the ratio of potentially beneficial vs. non-beneficial sequences decreases exponentially as well."
True but irrelevant when the functionally specific sequences can be reached with cumulative selection, from functionally weak and promiscuous sequences which are much easier to find. And which do not have to be generated by the slow accumulation of point mutations and/or single-nucleotide insertions over many generations.
"And, given their uniform distribution within sequence space, the minimum likely distance between a given steppingstone and the next closest potentially beneficial steppingstone"
Their distribution isn't known to be uniform, nor that they are actually "stepping stones" separated by these imagined seas of lethality or nonfunctionality you imagine. Once again, you are unwarrantedly extrapolating from the set of known protein functions into all of protein sequence space. You can't do that.
"...When you contrast this with the perfect vacuum of evidence supporting the existence of intelligent designers who can do what ID folks say they can do, it becomes clear why scientists are all but unanimous in preferring evolution over intelligent design."
Both sides; supporters of evolution and ID require faith. How much faith? It all depends what side you are on.
There is one problem though with this argument; the supporters of evolution try to ignore the fact that their theory is based on faith and not on scientific, experimental evidence.
At the same time the supporters of evolution demand scientific, experimental evidence from the ID supporters even though their support is clearly based on faith and ID inference-not the same thing as scientific, experimental evidence.
I would argue though that ID supporters have a better, much better case for ID than the supporters of evolution have for theirs.
While Rosenhouse is a mathematician, he really doesn't understand biological complexity
I think we can all agree he doesn't "understand" it the way *you* do. Sorry, but we've seen your "lottery fallacy" before. Hint: The odds against winning the Powerball jackpot are nearly 300 million to 1. So how do we get a winner every few weeks? If you get stuck, you could ask someone who understands probability math, like, umm, Jason Rosenhouse! :-)
And, that’s very easy to do since it is so statistically likely! – extremely easy in fact! It can be achieved in a handful of generations under the right conditions within a relatively small population of bacteria.
You either understand nothing about Lenski's experiment or are deliberately lying and banking on us not knowing enough about that experiment to call you on it.
At the same time the supporters of evolution demand scientific, experimental evidence from the ID supporters even though their support is clearly based on faith and ID inference-not the same thing as scientific, experimental evidence.
I have to say, it is very refreshing to see a supporter of Intelligent Design Creationism admit to the fact that ID is not supported by scientific evidence. Now, why don't you try going on Uncommon Descent or some other ID creationist website and arguing that. Tell us how long you last before they ban you.
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