I get lots of email from theists and creationists. They remind me that the controversies over religion and evolution are complicated. Here's a recent letter that illustrates the problem. It's from a creationist who struggles to incorporate his understanding of evolution into a worldview that just can't accommodate it. The results are .... interesting.
I really don't know to respond to this letter.1 Where does one begin when trying to correct such a profound misunderstanding of science?
I love your new definition of evolution as "a change in the frequency of alleles in a population over time." What happened to spontaneous and random mutations? Epigenetics blew that out of the water. I find it amusing every time I hear some evolutionists claim evolution is fact and the evidence is "overwhelming." Evolutionists have given up on fruitless attempts to prove the impossible and have implemented a new strategy of just claiming evolution has been proved by mountains of evidence.
Epigenetics proves adaptation and nothing else. It controls gene expression driven by environmental stress. It, nor any of the other theories of evolution provide for mechanisms to increase information in genomes. Hence evolutionists are confined to wild extrapolation of adaptation to prove macro evolution. Why hasn't it occurred in experiments? 50,000 generations of bacteria and still no macro evolution nor even proof of a simple DNA change much less added information in the genome. Guess why? You can't get there from here. Evolutionists look like idiots trying to make a plausible explanation why provisions for adaptation reside in what they call "Junk DNA" for millions of years before the organism is exposed to environmental changes that calls upon for them to survive.
The next time you consider calling someone an idiot you might consider there are some reading your posts that are not impressed by your insane unfounded conclusions. Allele frequencies are not going to hide the obvious shortcomings of evolution theory. Proving allele frequencies change proves epigenetics and adaptation and nothing else unless you are an idiot.
Don Berry
I have the sense of the common cow who knows how to eat the grass and spit out the cockle burrs.
1. I do not publish email messages without first obtaining permission from the author.
239 comments :
«Oldest ‹Older 201 – 239 of 239Here is the article that Jud was referencing:
http://www.ncbi.nlm.nih.gov/pubmed/17209030
"When the Lac- strain of Escherichia coli, FC40, is incubated with lactose as its sole carbon and energy source, Lac+ revertants arise at a constant rate, a phenomenon known as adaptive mutation. Two alternative models for adaptive mutation have been proposed: (i) recombination-dependent mutation, which specifies that recombination occurring in nongrowing cells stimulates error-prone DNA synthesis, and (ii) amplification-dependent mutation, which specifies that amplification of the lac region and growth of the amplifying cells creates enough DNA replication to produce mutations at the normal rate. Here, we examined several of the predictions of the amplification-dependent mutation model and found that they are not fulfilled. First, inhibition of adaptive mutation by a gene that is toxic when overexpressed does not depend on the proximity of the gene to lac. Second, mutation at a second locus during selection for Lac+ revertants is also independent of the proximity of the locus to lac. Third, mutation at a second locus on the episome occurs even when the lac allele under selection is on the chromosome. Our results support the hypothesis that most Lac+ mutants that appear during lactose selection are true revertants that arise in a single step from Lac- cells, not from a population of growing or amplifying precursor cells."
The authors show that alternative (ii) is not the explanation.
This dos not mean that alternative (i) is correct.
There are more than these two alternatives.
By showing that (ii) is not the explanation it does not in any way show that (i) is correct.
I have presented the idea that adaptation (adaptive mutation) could take place throgh the following steps:
1. The organism adapts to the environment through epigenetic means. And these epigenetic changes are passed from generation to generation.
2. After a certain number of generations, the epigenetic changes are passed to the nucleus through reverse transcription. And these changes (these adaptations) become fixed.
Anonymous quoted and bolded the following from Wikipedia regarding research by Barry G. Hall:
Hall later determined that his mutants were the result of transposon activity, and concluded that his results were in fact about transposon biology, and not mutagenesis.
And the significance of this "difference" (between mutagenesis and transposons) would be what, exactly? I put "difference" in quotes because transposon activity is often itself considered a means of mutagenesis (see Wikipedia article on "insertional mutagenesis").
Under stress, bacteria have been observed to allow increased numbers of errors in genome replication through both decreased DNA repair activity (which I presume the article you quoted calls mutagenesis) and through a decrease in level of factors that normally "silence" transposons.
While it is ordinarily adaptive to make genome replication as error-free as possible, under stressful conditions to which the organism is by definition not adapted, allowing random errors may permit more rapid adaptation to the new environment than normal more error-free replication.
Of course even an increased error rate may not allow rapid adaptation - in Richard Lenski's experiments, it took ~25,000-31,000 generations, IIRC, for the genomic mutations that allowed citrate metabolism to occur. So much for any notion that mutations can simply be directed non-randomly toward desired new capacities (unless someone wants to contend Lenski got a bunch of lazy "surfer bum" E. coli without sufficient mutational ambition).
Anonymous writes:
I am coming to see that I am wasting my time responding to every misunderstanding you come up with.
If you consider quote-mining various Wikipedia articles to be "responding," and my summaries of the actual research those articles are referencing to be "misunderstanding," I can see how you would feel that way.
There are more than the two alternatives that were labeled (i) and (ii).
Showing that alternative (ii) is not correct, does not imply that (i) is correct.
I have given another alternative that others like Steele have been researching.
It would appear that Hall is talking about retrotransposons (not DNA transposons).
Retrotransposons operate via reverse transcription.
I have presented the idea that adaptation (adaptive mutation) could take place throgh the following steps:
1. The organism adapts to the environment through epigenetic means. And these epigenetic changes are passed from generation to generation.
2. After a certain number of generations, the epigenetic changes are passed to the nucleus through reverse transcription. And these changes (these adaptations) become fixed.
To take this a further level of detail:
Possibly when the epigenetic change is passed to the nucleus it is stored as what is called a "pseudogene". ("Pseudogene" is not a very good name for it actually. I will call it an "override gene".)
The "override gene" stored in the nucleus, is automatically called into action whenever the main gene is activated. It regulates the creation of the messenger RNA that is created. (It acts as an override).
The modified (overridden) messenger RNA is then sent out into the cell to code the protein.
The net effect is that the epigenetic change is now firmly encoded in the DNA and operates there.
In support of these ideas consider the following:
http://en.wikipedia.org/wiki/Pseudogene
"There are three main types of pseudogenes, all with distinct mechanisms of origin and characteristic features. The classifications of pseudogenes are as follows:
Processed (or retrotransposed) pseudogenes. In higher eukaryotes, particularly mammals, retrotransposition is a fairly common event that has had a huge impact on the composition of the genome. For example, somewhere between 30% - 44% of the human genome consists of repetitive elements such as SINEs and LINEs (see retrotransposons).[6][7] In the process of retrotransposition, a portion of the mRNA transcript of a gene is spontaneously reverse transcribed back into DNA and inserted into chromosomal DNA.
And
It has been established that quite a few pseudogenes can go through the process of transcription, either if their own promoter is still intact or in some cases using the promoter of a nearby gene; this expression of pseudogenes also appears to be tissue-specific.[4] In 2003, Hirotsune et al. identified a retrotransposed pseudogene whose transcript purportedly plays a trans-regulatory role in the expression of its homologous gene, Makorin1 (MKRN1) (see also RING finger domain and ubiquitin ligases), and suggested this as a general model under which pseudogenes may play an important biological role.[19]Other researchers have since hypothesized similar roles for other pseudogene.
Let me clarify this:
There are more than the two alternatives that were labeled (i) and (ii).
Showing that alternative (ii) is not the explanation, does not imply that (i) is the explanation.
I have given another alternative that others like Steele have been researching
In response to Anonymous' most recent comments:
I have given another alternative that others like Steele have been researching.
Oh, you mean Ted Steele, whose research findings others could not reproduce, and who was eventually dismissed from his position?
Look, no matter how many Wikipedia articles you cut-and-paste portions of, surely you must know that this is not where groundbreaking research in evolutionary biology and genetics will be found.
And even more fundamental, if you did find groundbreaking research, it wouldn't support Lamarckian inheritance of acquired traits through any mechanism, including epigenetic changes retro-transposed, as a significant driver of evolution (except for the quite specific and well-recognized exception of horizontal gene transfer in bacteria and plants). If Steele was right that acquired immunity could be passed through inheritance, then why do millions get sick every year from diseases like measles for which their parents acquired immunity? Why did we need to develop vaccines, and why did they decrease the incidence of disease so dramatically?
Before throwing yet more steps of yet more hypothetical mechanisms against the wall in the hope that something will stick, show me careful, repeatable research (actual research publications please, *not* snippets from Wikipedia!) that demonstrates the end result of these hypothetical mechanisms - inheritance of acquired traits - actually occurs with sufficient frequency to be significant in evolution, other than the specific exceptions noted above. And further show me careful, repeatable research that demonstrates this significant activity is directional rather than random.
And finally, please also account for why, if evolution is so efficient and directional, it takes E. coli in a high-stress environment 25,000 generations or more to evolve citrate metabolism.
Jud, your post contains a number of false implications.
For example, Steele was dismissed for a reason having nothing to do with the topic we are discussing.
And if that is not enough, he was re-instated for unfair dismissal.
You are distorting the facts.
http://en.wikipedia.org/wiki/Edward_J._Steele
"The University of Wollongong subsequently appealed the court's decision, but again lost and was ordered to pay Steele's court costs (estimated to be approx. A$40,000). The University set out with further investigations into the allegations of soft marking in an effort to legitimately incriminate Steele, however there appeared to be a conflict of interest with Steele's former line manager being promoted to Dean, and chair of a subsequent enquiry. This led to Steele describing the UoW arbitration system as a 'Kangaroo court'.[8]
The unfair dismissal issue was resolved on 6 July 2002 when Steele and the University of Wollongong came to a confidential agreement. Although little is known in regard to the settlement, Steele did not return to the University of Wollongong.[9] Further reading.,[10][11]
Steele is currently based at the Genomic Interactions Group & CILR at the Australian National University."
You argue by means of character assassination - not relevant facts.
Also his work has been supported by others. Read the wikipedia article.
I am not arguing with your falsehoods. I am not wasting my time like that.
I have not studied this aspect of the subject very much yet, but the following is interesting:
http://www.medicinenet.com/measles_rubeola/page2.htm
"Those people at high risk for measles include:
children less than 1 year of age (although they have some immunity passed from their mother, it is not 100% effective)"
You argue by means of character assassination
Are you ignoring my mention of the fact that Steele's results could not be replicated?
Anonymous writes:
"Those people at high risk for measles include:
children less than 1 year of age (although they have some immunity passed from their mother, it is not 100% effective)"
And you think this immunity is genetic in nature??!!
Think for one second and ask yourself why immunity isn't passed from the father, who contributes half the child's genetic material.
Think for one more second and ask yourself what connection between mother and child could be responsible for this immunity that wears off within a year from birth.
Quote mining and sheer wrongheaded speculation like this aren't helping to convince anyone of flaws in evolutionary theory.
Here is what was said earlier about the Lenski experiment:
"Yep, now you can explain why those billions upon billions of E. coli didn't bother to develop those "epigenetic" changes for 30,000 generations. And why, after thousands of succeeding generations, now the majority of them suddenly have the ability to create these "epigenetic" changes. Were the first 30,000 generations "slackers" that just didn't want to change badly enough?"
For the first 30,000 generations they had enough food. No stress, no new gene expressions. As the grew larger (that's what the experiment was about according to Moran) they needed more food. Did it ever occur to you that larger organisms consume more food?
Is it correct that for the first 30,000 generations they had enough food?
Anonymous quotes faultfinder:
For the first 30,000 generations they had enough food. No stress, no new gene expressions. As the grew larger (that's what the experiment was about according to Moran) they needed more food. Did it ever occur to you that larger organisms consume more food?
And asks:
Is it correct that for the first 30,000 generations they had enough food?
No. Thank you at least for asking.
Quoting the first of the three mutually contradictory explanations of the Lenski experiment faultfinder gave earlier in this thread is no way to move the discussion forward. Before we go round and round again through all this slowly, let me just give those three mutually contradictory explanations:
- The stress and consequent epigenetic changes were greatest at the beginning of the experiment.
- The stress and consequent epigenetic changes were greatest at the end of the experiment.
- The changes occurred due to genetic mutation.
The last of the three is the correct explanation. Quoting from a paper by Lenski and colleagues reporting the experiment:
No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations....
Lenski and colleagues identified the precise mutations in the pykF and nadR genes that enabled the single variant strain, among all the various E. coli populations, to metabolize citrate.
I'd highly recommend you read the paper, cited by Dr. Moran earlier in this thread, rather than relying on anyone else's summary, mine included. And you could do a lot worse than read the many other publicly available things Dr. Lenski has written. It's fascinating stuff and tremendously educational.
Jud, since your posts are filled with falsehoods, I no longer take them seriously and waste my time on them.
You do not support your points with actual specific references so I am not wasting my time determining where you are distorting the facts.
Could someone else answer my question?
Jud:
"The stress and consequent epigenetic changes were greatest at the end of the experiment."
This confirms what I thought, and apparently what faultfinder was saying.
The stress and the adaptation occurred quickly at the end of the experiment.
That is what I would have predicted according to the ideas I have been presenting.
And that is consistent with the other experiment:
"The hypothesis was first proposed in 1988 by John Cairns, of Harvard University,[citation needed] who was studying Escherichia coli that lacked the ability to metabolize lactose. He grew these bacteria in media in which lactose was the only source of energy. In doing so, he found that the rate at which the bacteria evolved the ability to metabolize lactose was many orders of magnitude higher than would be expected if the mutations were truly random. This inspired him to propose that the mutations that had occurred had been directed at those genes involved in lactose utilization.[1][2]"
Here is a very significant observation in the Lenski experiment:
http://www.pnas.org/content/105/23/7899.full
"For example, the insertion of a mobile genetic element creates new sequences at its junctures, and one of these new sequences might then undergo a mutation that generates a final sequence that could not have occurred without the insertion. The E. coli genome has many insertion-sequence elements (53), some of which have been active in the LTEE (54–56). Whatever the mechanism, this potentiation made the Cit+ function mutationally accessible, and a weak Cit+ variant emerged by 31,500 generations."
Just as I would have predicted.
Here is an article by Barry Hall with a very interesting title:
http://www.springerlink.com/content/v76h259x22844541/
"Adaptive mutagenesis: a process that generates almost exclusively beneficial mutations"
For those interested, here is an interesting video on Ted Steele:
http://video.google.com/videoplay?docid=830139582673220790#
Anonymous writes:
Here is a very significant observation in the Lenski experiment:
[quote snipped]
Just as I would have predicted.
Wow! Surely there's a job waiting for you in Lenski's lab! And I'm sure he, as an evolutionary biology, will be pleased to know you agree with the way his research is pointing.
Please tell us what his forthcoming papers will conclude, I don't want to have to wait until he writes them.
Anonymous writes:
Here is an article by Barry Hall with a very interesting title:
http://www.springerlink.com/content/v76h259x22844541/
"Adaptive mutagenesis: a process that generates almost exclusively beneficial mutations"
Oh hey, but don't stop there, with just a title of one article! Let's get to the real crux of the matter. Here's an article cited on that same page that cuts right to the heart of the matter:
"The origin of adaptive mutants: Random or nonrandom?" by Paul D. Sniegowski.
Bet your intellectual curiousity makes you eager to find out which it is, right? Well rest assured, you won't be disappointed. The abstract makes it surpassingly clear what the conclusion is:
Several recent reports have claimed that adaptive mutants in bacteria and yeast are induced by selective conditions. The results of these reports suggest that mutants can arise nonrandomly with respect to fitness, contrary to what has been widely accepted. In several cases that have received careful experimental reexamination, however, the detection of seemingly nonrandom mutation has been explained as an experimental artifact. In the remaining cases, there is no evidence to suggest that cells have the capacity to direct or choose which genetic variants will arise. Instead, current models propose processes by which genetic variants persist as mutations only if they enable cell growth and DNA replication. Most of these models are apparently contradicted by experimental data. One model, the hypermutable state model, has recently received limited circumstantial support. However, in this model the origin of adaptive mutants is random; the apparent nonrandomness of mutation is merely a consequence of natural selection. The critical distinction between the origin of genetic variation (mutation) and the possible consequence of that variation (selection) has been neglected by proponents of directed mutation.
Ain't science wonderful?
You know, Anonymous, I am so glad you referred to the Lenski experiment once again, and cited the Barry Hall article on the same page where I found that wonderful Paul Sniegowski paper I quoted in my previous comment. Well, serendipity is a great thing, and wouldn't you know, Sniegowski and Lenski have published several papers together!
I know you will be interested to learn what Lenski himself thinks of some of the points you've been raising. In a paper entitled "Mutation and Adaptation: The Directed Mutation Controversy in Evolutionary Perspective," available in full at http://myxo.css.msu.edu/lenski/pdf/1995,%20ARES,%20Sniegowski%20&%20Lenski.pdf , Lenski and Sniegowski relate a classic experiment by Luria and Delbruck in 1943. In this experiment, Luria and Delbruck conclusively proved mathematically that resistance of E. coli to bacterial infection evolved through random mutation followed by selection, rather than inheritance of acquired immunity.
Isn't it great when you don't have to rely on speculation or intuition but can get a mathematically conclusive answer to a question you've been wondering about? I know you'll agree with me that it is. I'm sure you're relieved you won't have to go fetching more random quotes and article titles from around the Web now that we have the definitive answer from 68 years ago.
It's OK, you don't have to thank me.
For those interested consider the following analogy.
We have 1,000,000 rooms with stuff in each.
One of the rooms has a treasure in it.
One searcher looks through all the rooms randomly.
The other searcher is told that the treasure is in one specific room and he looks only through the stuff in that room.
Is the second search a "random search"?
For those interested consider the following analogy.
We have 1,000,000 rooms with stuff in each.
One of the rooms has a treasure in it.
One searcher looks through all the rooms randomly.
The other searcher is told that the treasure is in one specific room and he looks only through the stuff in that room.
Is the second search a "random search"?
Look at
http://myxo.css.msu.edu/lenski/pdf/1995,%20ARES,%20Sniegowski%20&%20Lenski.pdf
Take a look at the last paragraph on page 572.
For those who are interested in this subject you might be interested in the following talk by James Shapiro:
http://www.youtube.com/watch?v=gZOkfjuXDg4
Anonymous writes:
For those interested consider the following analogy.
We have 1,000,000 rooms with stuff in each.
One of the rooms has a treasure in it.
One searcher looks through all the rooms randomly.
The other searcher is told that the treasure is in one specific room and he looks only through the stuff in that room.
Is the second search a "random search"?
Nope, I wouldn't say the second search was random at all.
Look at
http://myxo.css.msu.edu/lenski/pdf/1995,%20ARES,%20Sniegowski%20&%20Lenski.pdf
Take a look at the last paragraph on page 572.
Glad you mentioned this. Here, let me quote most of that last paragraph:
By arguing that mutation is random, we have not meant to imply that mutation occurs at equal rates at all loci or in all environments, or that mutations do not have definable, proximate causes. Rather, we argue that environmental factors (proximate causes) do not induce specifically those mutations that are beneficial.
So environmental factors like stress don't specifically produce beneficial mutations - the "treasure" in your analogy. Rather, the best the organism can do is elevate the random mutation rate, which would be equivalent in your analogy to having the searcher run randomly from room to room, but faster.
Wow, so we agree! I never would have thought it.
Jud is missing the point they are making.
Does anyone else see it?
At least Jud understood one thing:
"Is the second search a "random search"?"
"Nope, I wouldn't say the second search was random at all."
It is not a random search.
The different rooms represent different parts of the genome.
The cell begins to make changes in the specific room (the specific section of the genome) that is relevant to the stress condition.
It undertakes changes through trial and error IN THAT ROOM. (Not in all the other rooms).
There is an element of direction - making changes only in that specific section of the genome. And there is an element of trail and error - the "random" changes within that section. Till it finds the right change in that section.
This is the idea I am suggesting.
It is what the evidence suggests, since the mutations do not occur at equal rates at all loci or in all environments and the mutations have definable, proximate causes.
http://shapiro.bsd.uchicago.edu/Shapiro.2009.GeneticsPerspective.pdf
"The second response to arguments against the natural
genetic engineering concept is to reflect seriously on
how living organisms are able to search effectively
through the infinite space of possible genome configurations.
The progenitors of extant organisms have had
to make these searches during the course of repeated
evolutionary challenges. So it should be no surprise that
today’s survivors possess evolved biochemical systems to
facilitate the evolutionary rewriting of genomic information.
These systems have the capacity to reduce the size of
the genomic search space dramatically and to maximize
the chances for success by using a combinatorial process
based on existing functional components. New combinations
of established coding sequences, transcriptional
regulatory signals, and chromatin determinants are far
more likely to prove effective than are a series of random
changes altering individual genetic elements."
Anonymous writes:
(1) The cell begins to make changes in the specific room (the specific section of the genome) that is relevant to the stress condition.
It undertakes changes through trial and error IN THAT ROOM. (Not in all the other rooms).
(2) It is what the evidence suggests, since the mutations do not occur at equal rates at all loci or in all environments and
(2) does not mean (1). You have made a leap unsupported by the evidence. There is nothing in the paper (and nothing in life) that connects the loci where mutations occur most rapidly with those involved in the specific operations of the organism that are being stressed. In fact, loci that have no effect on phenotype typically are among those that mutate most rapidly since there is no chance of an error affecting anything negatively.
The fact that mutation is non-directional, having been mathematically proved almost 70 years ago, is again very nicely illustrated by two series of experiments you've raised in this thread. (It is evident that in your rush to find anything quote-mineable to "prove" your point - since it was disproved mathematically, equivalent to insisting that 2+2 must and will equal 5 - you have either inadvertently or intentionally failed to fully consider and discuss the implications of the work you cite.)
In Barry Hall's experiments, E. coli evolved to metabolize lactose rather quickly. In Richard Lenski's, E. coli took nigh on forever - over 30,000 generations, the equivalent of 600,000 years for humans - to evolve to metabolize citrate. Is it because, to the undernourished E. coli or in the view of some designing/controlling entity, lactose metabolism was somehow tens of thousands of times more important than citrate metabolism? Anyone fair-minded will admit that is absurd, and plainly not a reasonable explanation for what was observed. It is because one of the three specific mutations needed to metabolize citrate is exceedingly rare, while the mutation that permits lactose metabolism "arise[s] in a single step from lac- cells."
If mutation occurred preferentially in the genes controlling the system under stress, thus "searching" efficiently and in a non-random manner toward the correct solution, then obviously the citrate metabolism mutations should have taken a length of time roughly the same order of magnitude as that enabling lactose metabolism. The fact that there is a several-order-of-magnitude differential is a very nice illustration of just how far off the mark your hypothesis is.
As Lenski and Sniegowski say in their paper (and anywhere else they've ever written on this issue), the mutations are random and the only thing that makes their impacts non-random is selection.
(3) the mutations have definable, proximate causes.
It would be quite strange if mutations didn't have causes, wouldn't it? How else would they ever occur? Some occur in a single step, some take 20-30,000 generations or more - y'know, like, random?
Jud ignores the fact that in the Lenski (citrate) experiment the organisms were not stressed until late and when stressed they adapted quickly.
But I am not arguing this again.
Shapiro's work provides abundant evidence for the fact that the cell itself is an intelligent agent.
And this is not a creationist issue.
There is another possibility.
If a survival change requires a set of changes, then it will take longer in the search to get the pieces together.
For example, if you are directed to the correct room there are still two possibilities within the search in that room.
One possibility is that you need to find only one item to obtain the treasure. That is relatively simple in the trial and error search WITHIN THAT ROOM.
The other possibility is that you need to find 3 items. That will take longer in the trial and error search WITHIN THAT ROOM.
Anonymous writes:
Jud ignores the fact that in the Lenski (citrate) experiment the organisms were not stressed until late and when stressed they adapted quickly.
But I am not arguing this again.
...he says, while arguing it yet again. :-)
Now remember that Anonymous is "not arguing" this because I pointed out that the E. coli in Lenski's experiment did not evolve the ability to metabolize citrate for over 30,000 generations. So when Anonymous writes that the "organisms were not stressed until late and when stressed they adapted quickly," he must mean somewhere very close to the 30,000 generation mark.
It's interesting, then, to read the scholarly paper Lenski and his associates published back in 2002, after "only" 20,000 generations had elapsed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC298728/). Actually, we don't have to read far. The very first sentence of the article says:
Twelve populations of Escherichia coli, derived from a common ancestor, evolved in a glucose-limited medium for 20,000 generations.
Thus the organisms were stressed from the very start by limitation of their normal food source. That was of course the idea of the experiment, to see what the evolutionary reaction would be from these E. coli under stress.
OK, Anonymous, care to throw out any other "facts" about Lenski's experiment without having bothered to read the articles he's written? Because the only other possibilities are that (1) you read but could not comprehend the experimental reports, or (2) you knew what the facts were and lied. I'm not going to accuse you of either of those things without good evidence, so for now I prefer to do you the kindness of assuming you knew nothing and just pulled your "facts" about the experiment out of your butt.
It appears that one mutation was required in the Cairns experiment and 3 interdependent mutations in the Lenski experiment.
It appears that one mutation was required in the Cairns experiment and 3 interdependent mutations in the Lenski experiment.
Is that correct?
If 3 interdependent mutations (changes) were required in the Lenski experiment, that would explain why it took longer.
That is consistent with what I am saying.
Jud had posted:
"If mutation occurred preferentially in the genes controlling the system under stress, thus "searching" efficiently and in a non-random manner toward the correct solution, then obviously the citrate metabolism mutations should have taken a length of time roughly the same order of magnitude as that enabling lactose metabolism. The fact that there is a several-order-of-magnitude differential is a very nice illustration of just how far off the mark your hypothesis is."
I have now answered that objection.
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