Monday, March 31, 2014

A creationist illustrates the argument from ignorance while trying to understand population genetics and Neutral Theory

I know I've said this before, but I continue to be astonished at the ignorance of creationists. Those who oppose evolution most vehemently don't understand it in spite of the fact that they are convinced it has to be wrong.

This is most obvious with the Intelligent Design Creationists because they like to use science-sounding jargon to convince us that they know what they are talking about. They claim that they can refute evolutionary biology using scientific evidence. Instead they just reveal their ignorance.

They've been doing it for decades in spite of the fact that many people have tried to educate them. I don't get it.

Recently, I tried to explain how the difference between the chimpanzee and human genomes is consistent with what we know about population genetics, mutation rates, and Neutral Theory. I was aware of the fact that this stuff would all be news to most Intelligent Design Creationists but it was still an opportunity to try, once again, to teach them about modern evolutionary theory.

Recall the the fundamentals of population genetics were worked out in the 1920s and 1930s and that Neutral Theory is about 45 years old. I think it's about time that Intelligent Design Creationists learn about them, no?

The only person to take up the challenge was a philosopher, Vincent Torley. Let's see how he does at: Fixation: the neutral theory’s Achilles’ heel?. He starts with,
The neutral theory of evolution appears to have won out over its rival, neo-Darwinian selection theory (see here and here). However, the neutral theory makes a very specific prediction about the rate at which mutations are fixed in a population, which I think warrants more testing and scrutiny. The evidence for this prediction which I’ve seen to date is frankly underwhelming.
There are several errors and/or misconceptions in this paragraph. First, Neutral Theory did not replace (win out over) natural selection. Neutral Theory refers to the fact that most new mutations may be neutral. If so, their frequency in the population will be governed by random genetic drift, described in the early 20th century. Random genetic drift is now seen as an important mechanism of evolution along with natural selection.

Second, Neutral Theory, per se, does not predict the rate of fixation of neutral alleles.1 That was what population genetics told us 80 years ago. What Neutral Theory says is that this may be the dominant form of evolution.

Third, I think we'll see that Vincent Torley never actually looks at the evidence for fixation of neutral alleles in a population so he really can't have an informed opinion.

Torley goes on to quote several internet sources in an attempt to understand, and explain, the concepts of neutral alleles and fixation rates. One of them is an article from talk.origins by Chris Colby. It's 20 years old. That's an indication of how long we've been trying to teach this stuff to creationists on the internet. The fact that Torley is relying on selected internet articles indicates that he doesn't have any books on evolution or population genetics. That's not a surprise.

Torley seems to get the idea that the overall rate of fixation of neutral alleles will be the same as the mutation rate per generation. That's just simplified population genetics. Now he's in a position to understand my post so he says ...
What Professor Moran is saying here is that 121 mutations are being fixed in the human population, in each successive generation. Since 185,200 generations have elapsed since the human and chimpanzee lines diverged, this means that 22.4 million mutations have become fixed in the human lineage since our ancestors diverged from the line leading to chimps. That’s a staggering number.
Since he can't be surprised by the number of generations, he must be "staggered" by the idea that there might be 121 new mutations per generation and that population genetics predicts fixation of 121 alleles per generation.

To his credit, he seems to have read (scanned?) my posts on the mutation rate in humans. Those are the post where I presented some of the evidence for the mutation rate.
Professor Moran thinks we shouldn’t be surprised. The rate of fixation is supported by three converging lines of evidence, as he explains, in a post titled, stimating the Human Mutation Rate: Direct Method (February 22, 2013):
There are basically three ways to estimate the mutation rate in the human lineage. I refer to them as the Biochemical Method, the Phylogenetic Method, and the Direct Method.

The Biochemical Method is based on our knowledge of biochemistry and DNA replication as well as estimates of the number of cell divisions between zygote and egg. It gives a value of 130 mutations per generation. The Phylogenetic Method depends on the fact that most mutations are neutral and that the rate of fixation of alleles is equal to the mutation rate. It also relies on a correct phylogeny. The Phylogenetic Method gives values between 112-160 mutations per generation. These two methods are pretty much in agreement.

The Direct Method involves sequencing the entire genomes of related individuals (e.g. mother, father, child) and simply counting the new mutations in the offspring. [Moran then cites a paper by Xue et al. (2009) which estimates the mutation rate at 103 mutations per generation.]
Now let's be clear here. What I'm doing is describing two methods of directly calculating the mutation rate. One of them relies on our knowledge of DNA replication and repair and the other relies on direct sequencing of parents and childeren and counting the number of mutations. The result is between 70 and 130 new mutations per generation.

The third method relies on our understanding of population genetics and the idea that most alleles are fixed by random genetic drift. When we plug in the numbers, we get a mutation rate that agrees with the direct measurements.

I did not present any independent evidence to support the idea the fixation rate is the same as the mutation rate. In the case of the Phylogenetic Method, I just pointed out that, if this were true (a reasonable assumption), then the mutation rate agrees pretty much with the other methods.

Vincent Torley says,
With the greatest respect to Professor Moran, none of these methods counts as an observation of the rate at which mutations get fixed in the human population. Inferring how many mutations must have taken place from an assumed time at which the human and chimp lineages diverged, is not the same thing as observing the rate at which mutations get fixed in the human line. And observing how many mutations occur in the space of one generation, from parent to child, is not the same thing as observing the rate at which mutations occur in the human population as a whole.
That's correct. My posts were about the mutation rate and not the fixation rate. However, the fact that humans and chimpanzees descend from a common ancestor several million years ago is just that, a fact. It would be perverse (IDiotic?) to believe otherwise.
Professor Moran might respond that according to the mathematical assumptions underlying the neutral theory of evolution, the rate at which mutations get passed on from parent to child is the same as the rate at which mutations get fixed in the population as a whole. That may be so; but it does not mean that an observation of the former automatically counts as an observation of the latter. The equation of the two rates only occurs within a particular theory of evolution: the neutral theory. If we are to test this theory properly, then, we need a population in which we can observe mutations getting fixed, and see if the rate accords with the mutation rate from parent to offspring.
Again, this is correct. It's population genetics theory that says the fixation rate should equal the mutation rate if the alleles are neutral. I was presenting evidence for the mutation rate.

The fact that the predictions of evolutionary theory and our knowledge of the mutation rate gives the right number for the number of differences between chimpanzees and humans, lends support to the theory but, strictly speaking, it is not a direct demonstration of fixation rates. (BTW, Torely never tells us the latest Intelligent Design Creationist version of population genetics so we can see if it works any better.)
Although I’m happy to be proved wrong, the claim that more than 100 mutations get fixed in the entire human population, in each passing generation, strikes me as implausible. I’m tempted to ask: where are all these mutations that are fixed in the human population in 2014, but were not fixed in the human population one generation ago, in 1987? Has anyone identified them?
A near as I can tell, this is all new stuff to Vincent Torley. He acts like he's never thought of it before. Judging by this paragraph, he has a lot more thinking to do. Perhaps, he should have done it before posting?
The time taken for these mutations to get fixed also seems extraordinary. We are told that for a population of N organisms, it takes (4*Ne) generations for a mutation to get fixed in the population, where Ne is the effective size of the human population. For most of human history, the effective population size appears to have been around 10,000, even though the actual human population size is thought to have been considerably higher (350,000 from the Middle Pleistocene onwards, according to a 2008 article by Professor John Hawks). Four times 10,000 equals 40,000 generations, and if we use Professor Moran’s figure of 27.5 years per generation, that’s equivalent to 1,100,000 years ago.

Let me spell that out: if we take a typical mutation out of the 100-odd mutations which (according to the neutral theory of evolution) got fixed in the human population within the last generation (from 1987 to 2014), we will find that that mutation first appeared in the human lineage some 1,100,000 years ago.

Am I the only one who thinks this figure is absolutely extraordinary? And for that matter, doesn’t the notion of a mutation that takes one million years to fix sound a little suspicious?
No, Vincent, you are not the only one who finds the basics of evolution "extraordinary" and "suspicious." Just about everyone who posts on Uncommon Descent and Evolution News & Views is as ignorant as you.

Do you really think the argument from ignorance carries any weight?
Should we trust mathematical estimates of how long it takes mutations to get fixed in the human population, given the enormous environmental upheavals (e.g. Ice Ages, the Toba eruption, and so on) that we’ve faced in the past million years?
The mathematics is solid. If Vincent Torley understood population genetics, he would realize that environmental upheavals don't make much difference.
And what about this? Anthropologist John Hawks estimates that positive selection in the past 5,000 years has occurred at a rate roughly 100 times higher than any other period of human evolution. He adds: “We are more different genetically from people living 5,000 years ago than they were different from Neanderthals.” All this hyper-evolution has been occurring at a time when the human population has been higher than ever before – which means that it should take much, much longer for mutations to get fixed in the population! So how does that work? Go figure.
John Hawks is probably wrong but in any case his argument is irrelevant. He's talking about the small number of alleles that might be fixed by natural selection and not the vast majority of neutral alleles that are fixed by random genetic drift.
Of course, I realize that testing the predictions of the neutral theory of evolution regarding how many mutations get fixed in the population in each generation, and how long it takes for a new mutation to get fixed, might be rather impractical for a long-lived, slow-reproducing species like Homo sapiens.

So I’d be very interested to hear from any readers with a biology background. How do the predictions of the neutral theory check out when applied to bacteria? What about simple eukaryotes? Have any studies been done for animals? Which ones? Over to you.
It's ludicrous to think that the people who comment on Uncommon Descent are going to help him. (Read the comments to see for yourself.)

Vincent Torley seems to think that population genetics and Neutral Theory are just idle speculations with no evidence to support them. That's very insulting to all the thousands of scientists who have been studying evolution for the past forty years. Does he really think that evolutionary theory rest on such a shaky foundation?

Fortunately for Torley, there are a number of papers that answer his question. The one that I talk about in class is from Richard Lenski's long-term evolution experiment. Recall that mutation rates are about 10-10 per generation. If the fixation rates of neutral alleles was equal to the mutation rate then (as predicted by population genetics) then this should be observable in the experiment run by Lenski (now 60,000 generations).

The result is just what you expect. The total number of neutral allele fixations is 35 in the bacterial cultures and this correspond to a mutation rate of 0.9 × 10-10 or only slightly lower than what is predicted. There are lots of references in the paper and lots of other papers in the literature.

Wielgoss, S., Barrick, J. E., Tenaillon, O., Cruveiller, S., Chane-Woon-Ming, B., Médigue, C., Lenski, R. E. and D. Schneider (2011) Mutation rate inferred from synonymous substitutions in a long-term evolution experiment with Escherichia coli. G3: Genes, Genomes, Genetics 1, 183-186. [doi: 10.1534/g3.111.000406]


1. We know that the modern theory is Nearly-Neutral Theory but that's a lesson for another time.

45 comments :

  1. Did you see the episode of Friends in which Ross tried to prove to Phoebe that evolution happens? He trotted out a mass of evidence, and her response was that she wasn't going to believe him, and the evidence didn't matter. I think we have something of the sort here. Torley's main argument, it seems to me, is "I don't believe it". Not much you can do there.

    Questions for population geneticists: what does "fixation" mean in a population in which every conceivable point mutation must be happening many times in each generation? And how does rapid population expansion affect the number of alleles fixed per generation?

    ReplyDelete
    Replies
    1. You can define fixation in that case as achieving a state where all copies of that site in the genome contain descendants of the particular mutant event, even though some of those may have since mutated again.

      That, or you can just say that any fixation will be temporary, if it occurs at all.

      Delete
    2. Whoa, Joe, there's a big difference between your two definitions of "fixation". What do you actually do? And in your calculations of fixation, do you count the rate of back mutation as a parameter?

      Delete
    3. This comment has been removed by the author.

      Delete
    4. It depends on the purposes of the calculation. If the piece of DNA is, say, a whole gene, and you want to know what the rate of change is, each change of a site is a substitution, even though the allele it gives rise to may change later at other sites.

      If the objective instead is to know whether the population will be have all sequences identical, then later mutations definitely do undo that.

      Delete
    5. My reply just now was to John, a thoughtful and knowledgable systematist who has raised a reasonable issue and deserves a serious reply.

      I have not a clue what LouiseG is saying.

      Delete
  2. Vincent Torley also wanted to set aside the models and use bacteria or yeast to ask empirically whether the rate of fixation, and the times of fixation, are as predicted.

    It would be very hard to sequence all members of a population, which is what he is asking for. In effect he is actually asking whether our models are exact descriptions of real populations. Because if the models were exact, the conclusions about fixation rates and times would be correct. Once you have a model that is precise, you don't verify its consequences empirically. For example, we do not prove the Pythagorean Theorem by measuring lots of triangles and seeing whether the hypotenuse is the square root of the sum of squares of the other two sides.

    Torley also expresses surprise that, in a population of 10,000 individuals whose generation times are 25 years would take 40,000 generations, or 1,000,000 years, to complete fixation of a neutral mutant, given that it fixes. That is what the theory says -- the population will take an average of 2 generations at each possible gene frequency between 1/(2N) and 1 - 1/(2N). It may seem counterintuitive that it would take that long, but keep in mind that the gene frequency meanders back and forth -- it is not in singlelinded pursuit of fixation.

    ReplyDelete
    Replies
    1. Typo: "it is not in singleminded pursuit of fixation."

      Delete
    2. I ought to add that we don't need to know that our models are precise descriptions of nature. They inevitably aren't. The statistician George Box famously said that "Essentially, all models are wrong, but some are useful." They give us insight. We have adjustments such as effective population number to try to correct for inaccuracy of the model.

      The issue is not their perfection, but whether conclusions such as that fixation will take about 4N generations (for a neutral mutation) are roughly correct. Complications such as nonconstant population sizes or "selective sweeps" ("hitchhiking") in which nearby sites are under natural selection will alter this time, temporarily, but will not change the long-term rate of neutral substitution.

      Delete
    3. The way I see it, you simply cannot argue against a lot of the theory because it starts from totally uncontroversial premises (how Mendelian inheritance works) and from then on proceeds to derive results the way mathematics does. If you are going to argue against the theory, then you are basically arguing against mathematics, and that's not a fight you can win.

      That does not mean that certain theoretical expectations may never turn out not to match empirical observations, but it is usually not because the theory is wrong but because we do not have a precise understanding of the population genetic environment of the groups studied. And those cases are not that common, but when they do occur they are highly informative.

      Delete
    4. Vincent Torley has posted an update in which he concedes the point:
      I think it is fair to conclude that short-term studies, done with microbes, lend support to the neutral and near-neutral theories of evolution.
      That's quite remarkable, although I don't see why he resisted it in the first place, since he already accepted common descent of humans and chimps.

      Delete
    5. That "update" is rather interesting. He basically concedes the main points that Larry has made here, and in so doing refutes his entire argument. However, he doesn't actually say this explicitly. I wonder how many of his fellow IDiots will realize that the "update" is in essence a retraction, when it's not spelled out to them. And I wonder if it's just an accident that he didn't spell it out.

      Delete
  3. Rate fixing for mutations is just speculation beyond minor cases of modern man.
    anyways these mutations are minor things and not in any likely way lead to crossing thresholds in physical bodies worth writing home about.
    There is no reason to not see mutations provoked into being by other mechanisms anyways.
    Its all untestable speculation. Its philosophy.
    Theres nothing in this for a creationist to debunk as evidence. One is just being asked to debunk lines or reasoning from raw data.
    By the way perhaps these mutation rates are in a state of stasis?! PE ideas could throw a monkeywrench into the works here.
    Accelerated mutationism rates might be a option in such speculations.

    ReplyDelete
  4. Torley is the typical creationist. He knows he doesn't have to take a course in population genetics or crack open a textbook to learn this stuff. Just cherry-picking random internet sources (no need to worry about their correctness) is good enough! Geez, the intellectual laziness of these guys amaze me.

    In mathematics, we see a similar phenomenon with Cantor crackpots. They can't accept Cantor's proof of the uncountability of the reals for quasi-religious reasons, so they find more and more elaborate ways to doubt it, without every actually studying any mathematics or pointing out what line of the proof they disagree with.

    ReplyDelete
    Replies
    1. Wasn't Cantor himself one of the Cantor crackpots? I hear he tried to see the Pope to give him the message that his work on infinities had important theological implications.

      Delete
  5. Thanks Prof. Moran

    I'd really be interested in seeing you reply to this post if you have the time:

    http://www.uncommondescent.com/genetics/fixation-rate-what-about-breaking-rate/

    ReplyDelete
    Replies
    1. Sal Cordova! Yeah, he's probably right......

      Delete
    2. This quote comes from early in the post:

      Ok, so let’s do an experiment. Let’s subject bacteria or plants or any organism to radiation and thus increase the mutation rate mutation rate by a factor of 1 million or 1 billion. Do you think the above formula will still hold? We tried it in the lab, it killed the plants, and at some point rather than speeding evolution we are doing sterilization.

      OK, I don't really need to read the rest, do I?

      Delete
    3. Great lab work! He fixed 'em good and proper!

      Delete
    4. Nope, we don't. Sal's response is to completely sidestep the discussion and start blathering about what happens if the mutation rate is so high no amount of offspring can compensate for it.

      Who cares? The mutation rate ISN'T that high, so what does it matter what happens then?

      Delete
    5. Yes, Silly Sal's argument comes down to: "If you kill organisms with radiation, they no longer reproduce. Therefore God."

      Delete
    6. BTW, he's speaking hypothetically, right? This buffoon's not actually doing experiments with radiation, is he? Though if he was, that might explain some things....

      Delete
    7. @Mikkel Rumraket Rasmussen

      Okay I realise that it is difficult to take Sal Cordova seriously and that his initial thought experiment about subjecting bacteria to radiation is silly but if you skip over that and read further into the post, you will see him make two claims:

      1) "Current estimates of the number of bad mutations are well over 1.0 per human per individual"

      2) "Nobel Prize winner Hermann Muller who said a deleterious mutation rate of even 0.5 per individual per generation would be sufficient to eventually terminate humanity"

      So my question is: which of these is wrong and why?

      Delete
    8. What's a "bad" mutation and how bad is it? Sal gives no definition.

      There's a significant difference between a straight up lethal-before-reproductive-age mutation, or one which is deleterious when you reach your 50's(well over the age at which reproduction normally takes place), and one which gives you slightly weaker knees in your late 20's.

      The world just isn't as overtly simplistic as Sal makes it out to be, with "bad", "good" and "neutral" mutations.

      Delete
    9. You'd think actual population geneticists have thought about questions like these, and you'd think someone who wishes to critically examine the merits of population genetics would familiarize himself with the work.

      Has Sal done that? Nope.

      Delete
    10. Mikkel Rumraket Rasmussen said:
      There's a significant difference between a straight up lethal-before-reproductive-age mutation, or one which is deleterious when you reach your 50's(well over the age at which reproduction normally takes place), and one which gives you slightly weaker knees in your late 20's.

      In fact, no there is not. It does not matter how severe the deleterious mutation is, because mildly deleterious mutations are permitted to rise to higher frequencies, resulting in the same genetic load. This is known as the Haldane-Muller principle. This has been discussed elsewhere on this blog.

      Delete
    11. @hariseldonian,

      It hardly matters which is wrong, does it? If the rate of "bad" mutations is over 1 per individual, since the humanity has not disappeared from the face of the earth, then the second premise is wrong. Or the second premise disproves the first. Either way, Sal the Stupid can't make an argument based on their both being true.

      Delete
    12. hariseldonian asks
      which of these is wrong and why?
      The first one, because it is based on the following premise:
      Using Larry’s low figure of 56 and generously granting that only about 11% of those are bad, we end up with 6 bad mutation per individual per generation
      But that figure of 11% is probably too high, because a lot of our genome is non-coding.

      Delete
    13. But that figure of 11% is probably too high, because a lot of our genome is non-coding.

      Don't let Larry hear you say that. You have just confused "non-coding" with "junk". I think you meant to say the latter.

      Delete
    14. "In fact, no there is not."

      Of course there is. If you're born without a heart, you're dead before reproductive age. If all "bad" mutations were really that bad, their frequency would have to be extremely low to allow the persistence of the species.

      So if the frequency of "bad" mutations really is over 1 per individual, the degree to which it is bad and at what point during the life history of the carrier it has an effect, is of paramount importance.

      That's not to say the question is resolved by simply postulating that deleterious mutations aren't outright lethal before reproductive age, as you rightly say it would just allow us to carry more deleterious mutations before the effect stacks up through some number of generations.

      Either way, we're not on our way to go extinct, which should give Sal something to think about, because observational reality tells us there's something wrong with his simplistic model of evolution being reduced to a steady accumulation of deleterious mutations.

      Delete
    15. @Corneel

      I think he gets his figure that 11% are bad from the fact that about 11% of our genome is not junk and probably essential (see here: http://sandwalk.blogspot.co.uk/2008/02/theme-genomes-junk-dna.html).

      This is a mistake since it makes no allowance for neutral mutations.

      Prof. Moran writes about this here: http://sandwalk.blogspot.co.uk/2009/11/genetic-load-neutral-theory-and-junk.html

      But I don't understand why he only counts the 1.3% of our genome that encodes proteins (what about the other 10% - 15% of our genome that is conserved)

      Delete
    16. In any case, it's extra hilarious that Larry has a post with the exact same argument as Sal's from 2009 and Sal's yet to catch up.

      *sigh*

      Delete
    17. Yeah. I often hear this argument from creationists, but they never seem to spell out their explanation for what they claim the evidence shows (never mind the fact that the evidence doesn't show what they say it does.)

      If mutations are accumulating at a rate that should have long ago led our extinction as a species, then why does our species continue to thrive? Is Baby Jesus going thru our genomes and magically stopping the "bad" mutations? The why doesn't He stop all of them?

      Delete
    18. @lutesuite: Obviously it's because human beings have only been on the planet for 5000 years! :D

      We're reaching our natural expiry date with all of these mutations we're gathering.

      Delete
    19. @Mikkel Rumraket Rasmussen
      Yes, he is a slow learner. Larry's 2009 post was in response to an article of Sal Cordova, in which Sal made exactly the same argument, including animation of gingerbread men.

      @hariseldonian
      Ah, that explains where that number came from. In any case, the figure of 11% is not really "generous", as he claims it is.

      @John Harshman
      Oops. Yes, you're right. I hope Larry forgives me :-)

      Delete
    20. Ok, so let’s do an experiment. Let’s subject bacteria or plants or any organism to radiation and thus increase the mutation rate mutation rate by a factor of 1 million or 1 billion. Do you think the above formula will still hold? We tried it in the lab, it killed the plants, and at some point rather than speeding evolution we are doing sterilization.

      Heh heh. Someone argued that water was necessary for growth. So we drowned the bastards! Turns out they were wrong.

      Delete
    21. Heh heh. Someone argued that water was necessary for growth. So we drowned the bastards! Turns out they were wrong.

      Lol.

      Delete
  6. What evidence is there that 100000 or a million generation of random copy errors can turn a chimp ancestor into a human? How does another level of incoherence (random drift) help what random errors can't do? We have experimental evidence of what random processes can (can't) do.

    M. Behe:

    "Twenty-five years later the culture -- a cumulative total of trillions of cells -- has been going for an astounding 58,000 generations and counting. As the article points out, that's equivalent to a million years in the lineage of a large animal such as humans."

    "the bottom line is that the great majority of even beneficial mutations have turned out to be due to the breaking, degrading, or minor tweaking of pre-existing genes or regulatory regions (Behe 2010). There have been no mutations or series of mutations identified that appear to be on their way to constructing elegant new molecular machinery of the kind that fills every cell. For example, the genes making the bacterial flagellum are consistently turned off by a beneficial mutation (apparently it saves cells energy used in constructing flagella). The suite of genes used to make the sugar ribose is the uniform target of a destructive mutation, which somehow helps the bacterium grow more quickly in the laboratory. Degrading a host of other genes leads to beneficial effects, too."

    "Over the course of the project several of the dozen separate strains developed what is called a "mutator" phenotype. In English, that means that the cell's ability to faithfully copy its DNA is degraded, and its mutation rate has increased some 150-fold. As Lenski's work showed, that's due to a mutation (dubbed mutT) that degrades an enzyme that rids the cell of damaged guanine nucleotides, preventing their misincorporation into DNA. Loss of function of a second enzyme (MutY), which removes mispaired bases from DNA, also increases the mutation rate when it occurs by itself. "

    "Lenski is an optimistic man, and always accentuates the positive. In the paper on mutT and mutY, the stress is on how the bacterium has improved with the second mutation. Heavily unemphasized is the ominous fact that one loss of function mutation is "improved" by another loss of function mutation -- by degrading a second gene. Anyone who is interested in long-term evolution should see this as a baleful portent for any theory of evolution that relies exclusively on blind, undirected processes."

    ReplyDelete
    Replies
    1. This shows that under Behe's definition of "loss of function", everything can still evolve and Behe will still baffle IDiot minds by finding new and clever ways of calling it "loss of function".

      Yeah, whales evolved by loss of function mutations, they can no longer run around on land. Their flippers constitute the loss of arms and legs etc. etc.

      And here you are, being intensely impressed by a semantic relabeling.

      Thank you to M. Behe for telling us how evolution works, by one thing changing into another through a long series of modifications, which usually entail that the original thing's function is initially degraded. Why IDiots think this is somehow an argument against evolution is among the reasons why we call them IDiots.

      Delete
    2. Birds' wings are also loss-of-function, as those limbs don't work as legs anymore. Insect segments are loss-of-function since the multiple similar segments of their ancestors are now reduced to many fewer, most of which have lost the legs on the segment. Molluscs have mostly lost their segmentation, chitons and monoplacopherans excepted. Most plants no longer have any cells that have flagella.

      And humans? They lost most of their hair, a lot of their sense of smell, their tails. It just goes to show that all evolution is degeneration, and no progress is made.

      Delete
    3. Unknown,

      Can you point to one of the Behe's examples of the the Intelligent Designer (whom he calls "Jesus') actually causing a "gain of function" mutation?

      Delete
    4. And humans? They lost most of their hair, a lot of their sense of smell, their tails. It just goes to show that all evolution is degeneration, and no progress is made.

      And they also learned how to lessen their fear of the unknown by the invention of gods.

      But in fairness, by other means too.

      Delete
    5. It's interesting to hear Creationists explain how Evolutionary Change X is really a loss of function. By now, they've accumulated quite a list of changes which do not involve an increase of function; antibiotic resistance, the ability to digest nylon, and on and on. Given the sheer number and variety of evolutionary changes which do not require an increase in function, I can't help but wonder: What evolutionary changes do require an increase in function? Every time Creationists explain how Evolutionary Change X is really a loss of function, the list of evolutionary changes which must involve an increase in function is reduced by one. One has to wonder: Just how long is the list of evolutionary-changes-that-require-increase-in-function? And every time Creationists transfer a particular evolutionary change from the increase-in-function-is-required list to the list of evolutionary changes that can be accomplished by a loss of function, the more likely it becomes that no evolutionary changes require an increase in function.

      Delete
    6. The creationists get really excited about orphan genes. I assume that's because they are clear examples of the evolution of new genes with new functions? :-)

      (Actually, most "orphan genes" aren't really genes at all. Very few of them have been shown to have a biological function. But don't tell the creationists. It would spoil their fun.)

      Delete
    7. I would argue that duplication followed by functional divergence counts as an increase in function (though of course not of a kind that would make creationists happy).

      As regards spectacular examples of functional decrease as a creative force during an evolutionary transition, it seems that the loss of the actinodin genes and1 and and2 significantly contributed to the development of tetrapod limbs out of "abnormal" fins (with no rays):

      http://www.ncbi.nlm.nih.gov/pubmed/20574421
      https://www.benaroyaresearch.org/sites/default/files/biochemist-feb-2014-p23_27.pdf



      Delete