Death of a popular anti-ID argument
by KrauzeI've never used the Discovery Institute's list of scientists skeptical of Darwinism to argue for my views, but I must admit that it has helped expose some of the ID critics' misunderstandings. Like in this post from Time's Michael D. Lemonick. He writes about one of the signers of that list, Dr. Michael Egnor. Dr. Egnor is a professor of neurosurgery and pediatrics at State University of New York, Stony Brook and is named one of New York's best doctors by New York Magazine. Lemonick is not amused:
Yes, he actually is a brain surgeon, and yes, SUNY is a reputable place. Which is very important if you need your brain operated on, but which says nothing whatever about your sophistication about biological theory or about evolution. Discovery counts on your awe of brain surgery and your awe of magazine "best" lists to keep you from thinking about the fact that there's nothing here establishing Dr. Egnor's expertise on the topic at hand.
This is all true: Like most scientists, surgeons don't spend much time thinking about origins, as they don't need it in their day-to-day work. But did you notice that Lemonick just harpooned one of the critics' favorite arguments? If you ask the "pro-science" bloggers, any skepticism about orthodox evolutionary biology is "anti-evolution", and nothing in biology makes sense except in the light of evolution. But if this was correct, Dr. Egnor wouldn't even be a competent brain surgeon, let alone one of New York's best doctors. In pointing out that a brain surgeon has no particular expertise on the topic of evolutionary biology, Lemonick also helps us put our finger on the reason they have no such expertise: They don't need it to practice their profession.
As philosopher of biology Michael Ruse remarked: "When Dobzhansky said that nothing in biology makes sense except in the light of evolution, he was not just making an epistemological claim. He was making a political statement. A war cry to rally the troops."
February 18th, 2007 at 7:24 pm
Excellent point, Krauze. I only wish I thought your title, "Death of a Popular Anti-ID Argument," weren't so over-optimistic. This one won't die for a long time, even though it deserves to. The anti-ID crowd really need it, and they won't let go of it.
Comment by TomG — February 18, 2007 @ 7:24 pm
February 18th, 2007 at 7:32 pm
You're right Tom but it is helpful to point out logical inconsistencies and the use of an emotive rally cry on the part of the objective, it's about science, crowd.
Comment by Bradford — February 18, 2007 @ 7:32 pm
February 18th, 2007 at 7:41 pm
I wonder if Ruse was not overly harsh on Dobzhansky's statement. "Makes sense" can be understood multiple ways. I suspect Dobzhansky meant it in the sense of "why is it that way" whereas a surgeons idea of "sense" is much more pragmatic/functional in nature. Egnor may very well know how various functional capacities are arranged in the brain (i.e. knows what not to chop or drill, etc), but I doubt he'd be able to offer a good explanation of "why motor cortex is here next to X" whereas an evolutionary explanation, drawing on ancestral relationships, would fair better. Likewise, a physician could tell you the biological reason that hanging by rope is lethal, but evolution gives the historical quirks of our evolution that make us "hangable." And so on with human sinus problems, etc. So while Dobzhansky overstated his case when he said "nothing in biology," I don't think he was thinking about the kind of mechanics view of biology that Egnor uses. (Personally, I have my own doubts/biases about just how biologically or scientifically based cutting into brains currently is… In my experience, neurologists and neurosurgeons have a kind of "get out of jail free" card for diagnosis/surgeries b/c "brains are just so darn complicated" and, when it comes down to it, our state of knowledge remains somewhere in the dark ages)
Comment by great_ape — February 18, 2007 @ 7:41 pm
February 18th, 2007 at 8:02 pm
I just wanted to post one comment about these "lists" of scientists who are skeptical of evolution. From when I first started watching this debate, I've never seen Darwin-skeptics use these lists to argue that because such an overwhelming number of scientists doubt-evolution, that therefore you should to.
Rather, they are always used to rebut a common claim from Darwinists: "that no real scientists or academics question evolution" — who then use that false claim in an attempt to rhetorically shut down any discussion and debate on evolution. I've been told that Discovery Institute actually started its list a few years back precisely because a leading Darwinist had apparently claimed that no real scientists question evolution. I'm not sure if she still makes that claim in light of this list (though I'm sure she gladly makes fallacious appeals to authority by citing all the Steves).
In short, the point of these lists is more defensive than offensive. They are used to refute a common–and patently false claim–that no scientists question neo-Darwinism. The most repugant aspect of this false claim is when it is used to attempt to stifle scientific inquiry and classroom discussion. Anyways, that's my take on it.
Comment by Casey Luskin — February 18, 2007 @ 8:02 pm
February 18th, 2007 at 9:07 pm
As I understand it, your argument goes as follows:
If nothing in biology makes sense except in the light of evolution, then brain surgery does not make sense without evolution. Therefore, Dr. Egnor could not be a competent brain surgeon, because to him brain surgery wouldn't make sense.
You appear to accept that being skilled and knowledgeable about the contemporary practice of brain surgery does not require an intricate understanding of evolutionary origins. And you appear to accept that most scientists believe this to be so.
Therefore, you would obviously understand that most scientists would object to the logic, "If nothing in biology makes sense except in the light of evolution, then brain surgery does not make sense without evolution." (My paraphrasing of your argument.)
Now, we could talk about where we might find the fallacy in the sentence "If nothing in biology makes sense except in the light of evolution, then brain surgery does not make sense without evolution." But such a discussion would be needless because you've already accepted that it's not true, since "surgeons don't spend much time thinking about origins, as they don't need it in their day-to-day work."
Let A = "Nothing in biology makes sense except in the light of evolution."
Let B = "Brain surgery does not make sense without evolution."
You agree that A does not imply B. This does NOT mean that A is false. It simply means, in the context of A, that the implication does not follow. The "nothing in biology" is a metaphor which denotes the enormous volume of evidence which fits together like pieces in a puzzle under the theory of evolution. The phrase does not necessarily lend itself to a game of prepositional logic.
Consider this reasoning:
1. God is love.
2. Love is blind.
3. Therefore, God is blind.
This is just another example of the dangers involved in using metaphors literally.
Comment by jeff_alexander — February 18, 2007 @ 9:07 pm
February 18th, 2007 at 9:47 pm
He also undercut Dr. Dini and other critics, who tried to argue that you can't be a creationist and a good physician.
Comment by MikeGene — February 18, 2007 @ 9:47 pm
February 18th, 2007 at 10:41 pm
Ape…I think you might be reading into the quote by D-man to keep it afloat. In my Philosophy of Natural Science class at Texas A&M, i read a few articles by Ruse where he would quote this and just about every time he quoted it, it was in reference to practical application sciences. Of course, to use it in a way to answer the "why" question to our existence is effectively asking "how" in an atheistic/evolutionary paradigm, so pushing the referece back to the epistemological topic is essentially creating circular reasoning (that is, assuming evolution and then asking why and answering with "cause evolution is true") which removes all power from the quote. That's why I don't think Ruse would use it that way. Blessings!
Comment by Wayson — February 18, 2007 @ 10:41 pm
February 19th, 2007 at 12:03 am
Whoops! I mean, "That's why I don't think Do-guy would use it that way."
Comment by Wayson — February 19, 2007 @ 12:03 am
February 19th, 2007 at 2:21 pm
So, is anyone here willing to defend Egnor's ignorant and ridiculous claim that random mutation and natural selection can't produce new genetic information?
Comment by nickmatzke — February 19, 2007 @ 2:21 pm
February 19th, 2007 at 2:36 pm
Did he say that? I won't defend such claims, but it is not ignorant, because the on average change in specified information is that of a decrease, not increase.
It could be defensible if one regards the genome when going through duplications as a "lossy" decompression. When an 3 meg Mp3 decompresses to a 40 meg Wav file, is that really an increase of information?????
Gene duplications are suggestive of decompression, not information increase. But that is somewhat in the eye of the beholder.
Comment by Salvador T. Cordova — February 19, 2007 @ 2:36 pm
February 19th, 2007 at 2:51 pm
Hi Nick,
I certainly won't. Are you willing to defend a popular anti-ID argument?
Comment by Krauze — February 19, 2007 @ 2:51 pm
February 19th, 2007 at 4:01 pm
Sal — this is Egnor's main argument throughout his responses on Time magazine's blog. This is his Great Big Stumper Argument That Shows The Dogmatic Darwinists Are Dogmatic And Wrong. He's quite proud of it. Furthermore, "no new information" is a standard ID talking point, and the Discovery Institute proudly linked to Egnor's response this weekend. But it's just dumb, because the origin of new genes with new functions is reasonably thoroughly understood and widely available in the scientific literature — basically, duplications plus mutations plus selection (creationist/ID guys typically just focus on duplication, which again is ignorant). We debunked this ID claim in Kitzmiller and numerous other times. And yet here is the Discovery Institute's newest champion shamelessly promoting an unambiguously crank claim, and the Telic Thoughts blog citing Egnor as if his crankery didn't exist.
Krauze, if you agree that Egnor is flat wrong on his favorite pro-ID argument, then you've shown that the opinions of accomplished professionals can be worthless when they expound upon areas outside of their field without researching what they are talking about, and that the Discovery Institute and the ID movement are fools for citing Egnor.
As for your argument — if Egnor ever relied on an animal model, e.g. monkeys, in any of his work, training, or research that he based his work on, then he's wrong to claim that evolution wasn't important for his job. The fact that he doesn't realize its importance doesn't necessarily mean it wasn't important.
Comment by nickmatzke — February 19, 2007 @ 4:01 pm
February 19th, 2007 at 4:11 pm
Salvador T. Cordova said:
I won't wade into the whole "information increase" swamp, but I can easily address this quote.
In regard to raw data, decompression is not lossy. Compression is lossy (e.g. mp3), and can be lossless (e.g. zip).
The goal of a compression algorithm is to bring the data from a state of low entropy to a state of high entropy. The theoretical ideal compression algorithm would compress to a state of highest possible entropy: a statistically random set of data.
Thus the mp3 is smaller and has high entropy, while the wav is larger but has lower entropy (unless, of course, you are listening to pure noise).
You can do an experiment by starting with a statistically random set of data. Here's a short ruby script which produces a 10k file of random bits:
File.open("random.txt","w"){|f|10000.times{f.write rand(256).to_i.chr}}
If you compress this to random.zip, you'll find it is actually larger than random.txt (by 123 bytes in my experiment).
I'll leave the relationship between information and entropy to another day — or as an exercise for the curious.
Comment by jeff_alexander — February 19, 2007 @ 4:11 pm
February 19th, 2007 at 7:08 pm
Yes indeed Nick.
I would also like to question your use of "ignorant and ridiculous" here. Scientists (such as Egnor and yourself) have both the right and indeed the duty to question science that they find questionable. Science is all about questioning and scientist are not to be attacked for merely doing their work.
In 2004 I debated this issue on ARN and I consider it settled. Only one Darwinist (DJ Mullen) even showed up to the debate. The conclusion of the debate was that both Natural Selective Destruction (NS) and randomization (RM) are destruction functions wrt biological information.
From…03-09-2004 "Argument from the Logically Prior Superselection"
#1. "Natural Selection" as it is used in Darwinism, is a non-sequiter. The "origination" or "addition"(positive) of new species does not logically follow from Natural Selective Destruction (negative). No amount of killing (negative) of light peppered moths can produce (positive) dark colored moths. Killing and creating are logically and functionally distinct. Without the pre-existing genetic material for dark colored moths, NS would just kill them all. The active — change inducing — component of NS (and of any physical filter) is its blocking (negative) function. NS is therefore bio-complexity negative.
#2."Random mutation" is a garburation function applied to the genome. Randomization functions are destruction functions. Randomness is not a biological novelty producer. Randomness is a structure attenuator/destroyer. Randomness is not biological period ("full stop" in old english). Randomness is a mathematical function devoid of any biological meaning or syntax. Randomness is, by definition, insensitive to macroscopic order. Biological order is macroscopic. Randomness is therefore bio-complexity negative.
#3. "Reproduction" as it is used in Darwinism, is a physical copying function. In a platonic idealization, copying functions can be perfect (bio-complexity neutral). In the real world, however, no copying function is perfect and random copying errors are inescapable. Randomness is, by definition, insensitive(destructive) to macroscopic order. Biological order is macroscopic. Physical reproduction is therefore bio-complexity negative.
Comment by William Brookfield — February 19, 2007 @ 7:08 pm
February 20th, 2007 at 1:04 am
"…is essentially creating circular reasoning (that is, assuming evolution and then asking why and answering with "cause evolution is true")" =wayson
The how/why explanation that I envisioned from evolution consists of specific details about historical contingencies and selective constraints that resulted in the brain's lay-out being the way it is. That is, the explanation would be a set of information about the brain that is only derivable using an evolutionary paradigm. If I simply explained the observed brain by saying "because that's how it evolved," that would be as vacuous as saying "because that's how it was designed." The power of a theoretical framework consists in what informational fruits it yields. While it is clear to me what fruits are yielded from evolutionary theory, ID theory is not so clear, particularly because "design, "via adaptation, is already encompassed within evolutionary theory. We get no *new* benefit by limiting ourselves *strictly* to a engineering paradigm (i.e. ID) while at the same time we (at least some ID proponents, at least) throw out all the rich historical information, population phenomenon, etc, etc, that we've learned from working in the evolutionary paradigm.
Comment by great_ape — February 20, 2007 @ 1:04 am
February 20th, 2007 at 2:56 am
So, Brookfield, are you telling me that a mutation couldn't increase the amount of melanin in a peppered moth and turn it black? This is what your point #2 claims.
Argh. There are other things to say to nonsense like this, but it wouldn't be polite. Please go read about the Luria-Delbrück experiment. It contradicts all your claims including your multiple levels of misunderstanding of the term "random." They won a Nobel prize for it.
Comment by Nick Matzke — February 20, 2007 @ 2:56 am
February 20th, 2007 at 5:27 am
I laughed at this ignorant claim by Egnor:
The guy truly doesn't know what he's talking about when it comes to evolutionary theory. So having his name on the Dissenters from Darwininsm list is something the DI should probably not want made public. Oops. Too late.
Comment by KC — February 20, 2007 @ 5:27 am
February 20th, 2007 at 6:36 am
True to his political activism Nick Matzke decides to claim, using unwarranted extrapolation from limited evidence (e.g. Luria-Delbrück's Fluctuation Test), that evolutionary science has solved the problem of the origin of biological information and complexity.
One has to wonder if words like ignorant, nonsense or ridiculous, describing other views, are used to project his superior knowledge or his ultimate arrogance.
Comment by inunison — February 20, 2007 @ 6:36 am
February 20th, 2007 at 3:04 pm
Hi Nick,
"Krauze, if you agree that Egnor is flat wrong on his favorite pro-ID argument, then you've shown that the opinions of accomplished professionals can be worthless when they expound upon areas outside of their field without researching what they are talking about,"
I know. I said as much in my post.
"and that the Discovery Institute and the ID movement are fools for citing Egnor."
Yes, because if anyone disagrees with the Mighty Krauze about anything, they must be fools. Seriously Nick, has it ever occurred to you that not everyone shares your desire to vilify opponents? I may disagree with many of the things the DI does, but that doesn't mean they are fools.
Besides, do you want to count how many neurologists are on the Project Steve list?
"As for your argument - if Egnor ever relied on an animal model, e.g. monkeys, in any of his work, training, or research that he based his work on, then he's wrong that evolution wasn't important for his job."
Actually, model organisms are a funny example, as most of them clearly weren't selected with evolution in mind. As for monkeys, you don't need evolution to apply their biology to humans. The similarity between humans and monkeys were known long before Darwin ever set pen to paper.
Comment by Krauze — February 20, 2007 @ 3:04 pm
February 20th, 2007 at 10:29 pm
Surgeons practice their art on other animals prior to working on humans (indeed, this is how diabetes was figured out). Other animals are used because, evolutionarily, they are related to humans.
One can be an idiot about the history of one's profession, and one can couple that with incorrect denial of that history, and still be a competent technician in the field. That doesn't change the fact that scientists who got this fellow where he is used evolution theory to do it.
It does remind one of the story of the blind men who were healed by Jesus, and then forgot to say "thank you."
Comment by edarrell — February 20, 2007 @ 10:29 pm
February 20th, 2007 at 10:33 pm
edarrell:
My history might be wrong, but wasn't surgery practiced before the Theory of Evolution?
Comment by Bilbo — February 20, 2007 @ 10:33 pm
February 20th, 2007 at 10:52 pm
Nick before I get started I have one observation you must be really terrified of ID because only a person that is insecure would resort to the type of personal attacks you make on people you disagree with. I would like to point out the difference between you and another anti ID poster on this board ie Mesk.
I respect Mesk and I consider his or her's arguments. Mesk does not attack the person but the science. Mesk may or may not be wrong but Mesk is secure in himself you and others could learn from Mesk.
I have copied below the writings of Egnor that has the passage that you refer to as it relates to Egnor. Is this the writing of Egnor you pulled your quote from?
Vivid
Comment by Vividbleau — February 20, 2007 @ 10:52 pm
February 20th, 2007 at 10:58 pm
Hi Vivid. Good to see ya'.
Comment by Bilbo — February 20, 2007 @ 10:58 pm
February 20th, 2007 at 11:05 pm
I should say is this the writing you are asking pro ID people to defend or not defend?
Vivid
Comment by Vividbleau — February 20, 2007 @ 11:05 pm
February 21st, 2007 at 1:00 am
Nick,
Absolutely. The key issue is "organization", as opposed to "order". RM&NS cannot produce "organization", which I claim would be equivalent to "genetic information". (Not all "information" is equal.)
Oh, and you can't seriously be trying to say that an increase in the amount of melanin produced is tantamount to an increase in genetic information, can you? You're just joking, right? Of course not - that would be like saying an increase in height is evidence of evolution and the power of RM&NS.
Comment by Douglas — February 21, 2007 @ 1:00 am
February 21st, 2007 at 1:51 am
Maybe he isn't, but I will. The environment surrounding the moths altered, in such a way that moths with a higher level of melanin had a higher reproductive fitness than those with lower levels. Mutations increasing the level of melanin (whether pre-existing or novel) thus increased in frequency over time until they came to dominate the population, substantially altering the average colouration of the population as a whole.
In information terms, information about the environment was transferred by selection into the genome of the moths. This is pretty obvious: if all you had to work with was genome sequences from the moths, you could get a much more accurate picture of their environment after the selective event than before it - so information about the environment must have been added to the genome. That's an increase in genetic information, pure and simple.
Evolution isn't a magical force that creates information from scratch - it simply copies it from one place (the environment) to another (the genome). And in doing so it increases the information content of the genome.
Comment by Mesk — February 21, 2007 @ 1:51 am
February 21st, 2007 at 2:57 am
Mesk,
Are you claiming that two varieties of moth (the typica or white variety and the carbonaria or black variety) did not exist prior to industrial pollution?
To paraphrase Taylor:
and Majerus in "Melanism: Evolution in Action" offers another possibility:
I'm afraid this is another old classic that won't go gracefully.
Comment by inunison — February 21, 2007 @ 2:57 am
February 21st, 2007 at 3:00 am
Hi Bilbo ditto. I see your now a big "mucky muck"
Vivid
Comment by Vividbleau — February 21, 2007 @ 3:00 am
February 21st, 2007 at 4:55 am
Bilbo,
Sure, surgery was practiced prior to understanding how and why it worked. The use of animal analogs really took off after it was understood that the analogs had a scientific basis.
Eggs were cooked prior to the understanding of why heat changes the texture of the egg — but that doesn't make the chemistry wrong.
Modern surgery is the result of experimentation with animals. Animals are used because they are, evolutionarily, linked to humans. As anyone who does research with animals can tell you, a serious issue in such research is whether the scientific analogy is valid. For various animals, the analogy may be less valid than others. For example, many mammals still manufacture their own vitamin C, and don't need daily doses of it like humans and guinea pigs. Rats and mice are not particularly susceptible to Hansen's disease, so research on that disease was delayed until a suitable animal analog was found (turned out to be armadilloes).
In recent years we've seen the hullabaloo over the use of goats in trauma surgery research. In order to study how better to treat humans wounded on battlefields, animals were wounded the same ways, to study how to stop the bleeding, suture the wounds, etc.
Certainly someone could master the use of a scalpel and rely on the research of others to be a competent surgeon — that's part of the idea of having the research done and published in the first place.
But that this one surgeon seems so totally plug-ignorant of the history of his profession doesn't mean the history doesn't exist.
I often wonder whether creationists have a mutation or a virus which interferes with understanding of evidence and how it is used. This would explain creationist bravado prior to the many trials they lose, and why creationists, handed the keys to getting creationism into textbooks in 1982, have never bothered to use them.
Comment by edarrell — February 21, 2007 @ 4:55 am
February 21st, 2007 at 5:38 am
Ed: Modern surgery is the result of experimentation with animals. Animals are used because they are, evolutionarily, linked to humans.
Animals are used because it is unthinkable to use humans for experimental purposes this side of the Third Reich.
Comment by Bradford — February 21, 2007 @ 5:38 am
February 21st, 2007 at 6:34 am
Nope - I said, "Mutations increasing the level of melanin (whether pre-existing or novel)". I don't claim to be an expert on the peppered moth story - but as I understand it, while there's every chance that the darker morph existed at low frequency prior to the existence of industrial pollution, but there's no question that that frequency increased substantially once the pollution arrived.
Comment by Mesk — February 21, 2007 @ 6:34 am
February 21st, 2007 at 7:00 am
inunison,
In your quote from Melanism: Evolution in Action, is Majerus actually talking about the peppered moth? This site seems to suggest that he's referring to other lepidopterans, but as I don't have access to his book I can't check.
Comment by Mesk — February 21, 2007 @ 7:00 am
February 21st, 2007 at 8:34 am
Mesk, you are correct re: Dr. Majerus quote. On page 68 he discusses another mechanism of evolutionary change in connection with an other Lepidoptera.
This work is very interesting. Dr. Majerus attaches great importance to Kettlewell's work on melanism,
but on the other hand he points out deep problems with the conventional interpretation of peppered moth melanism in terms of the NDT, like non-existence of important bird predation evidence (p. 125) and scarcity of data on resting sites in the wild (p. 121).
While I do not deny that RM+NS could account for industrial melanism of the peppered moth, I really don't see basis for your claim that it "increases the information content of the genome."
Are you saying mutation(s) is not random in this case?
Comment by inunison — February 21, 2007 @ 8:34 am
February 21st, 2007 at 10:43 am
Not at all. Mutations occurred randomly, some of which conferred increased melanism. In the new environment, these variants were favoured and increased in frequency. The end result is a population that better matches its environment; in other words, information about the environment has been transferred into its genome.
There's no requirement for non-randomness or intention - random mutation coupled with non-random selection (which is the conduit for transfer of information from environment to organism) is sufficient.
Comment by Mesk — February 21, 2007 @ 10:43 am
February 21st, 2007 at 12:34 pm
Mesk:
Um… I am not seeing how you manage to get "information about the environment" from selection of an inherent trait over generations. If information is data in intelligible (or translatable) form, it must be something the information processor (in this case, the moth) can make use of for its own survival or to guide its own processes.
What does the existence of 'extra' melanin genes (or enhanced expression suites) tell the moth about its environment? In what way does the moth's expression of pre-existing genes inform the moth that "bird" will eat it if it doesn't park on dark bark (which isn't where such moths generally park in the first place)?
I'm just confused. I do consider sensory data to be "information," most times readily processed by the organism and sometimes (depending on the information) used to trigger responses that are themselves internally-generated biochemical suites. I know of no research that suggests these moths are chameleon-like in being able to vary their melanin genes or expressions based on the presence or absence of predators in the environment. Nor do I know of any researchers who claim that egg-laying moths alter the melanin genes of their offspring in reaction to the presence of birds who can pick light-colored moths easier than dark-colored moths.
Thus there is no discernable "information about the environment" present in the coloration of the moths. You - a human - may suppose (and obviously do suppose, because that's what this argument has always been about) that YOU can discern information about the moth's environment from its color, but that doesn't make your supposition actual "information," and it doesn't make the "information" available to either the moths or the birds. The gene codes for protein, that's all. You can't unfold it and read from the aa sequences ANY "information" about the habits of moth-eating birds. You can decode the gene to match the aa sequences in the finished product, and it doesn't tell you anything about moth-eating birds either.
Let's not confuse RM-NS with "information" or with any projected just-so stories about "information." These are the simplistic mechanisms of evolution postulated by a simplistic nineteenth century theory about how life evolves. It does not and never did say anything meaningful about "information." That was genetics' accomplishment, and it says nothing about environmental "information" as part of the base coding.
Comment by Joy — February 21, 2007 @ 12:34 pm
February 21st, 2007 at 1:27 pm
Joy — the environment turned black, and subsequently the moth population turned black to match. The moth genome now encodes information about the environment.
If you don't like this, give us a rigorous definition of "information" that enables us to determine what parts of the genome contain information, and which don't. The universal problem with antievolutionists/anti-Darwinists whining about "information" is that they can never give a rigorous definition of "information", yet they make their own fuzzy mystical view of it the core of their argument.
PS: Clarifications on Majerus:
1. In that quote someone posted, Majerus was talking about other kinds of melanism. Melanism in the peppered moth is known from breeding experiments to be a standard genetic trait following Mendelian inheritance.
2. Majerus argues strongly in his book that industrial melanism in the peppered moth had a point origin by mutation in the 1800s. There is no actual evidence that the melanic trait existed at any frequency above the background mutation rate before that. The issue has become confused because (a) Kettlewell argued that melanism (in general, across the many moth species he studied — not specifically for peppered moths) was a trait that had gone up and down in frequency over thousands of years due to environmental changes like fir forests and (b) creationists, desperate to claim that mutations can't be beneficial and can't create new information, have endlessly repeated the claim that the melanic trait was already present in the moth population when soot pollution began in England.
But no one has yet done the molecular biology that would be required to identify and sequence the melanism gene and figure out exactly what happened and if it happened more than once.
3. The idea that Majerus overturned Kettlewell's experiments and his explanation for melanism is a horrifying distortion of Majerus's actual views and writings, propagated by a combination of overhyped news reports and creationist propaganda. No one is more horrified by this than Majerus himself.
Comment by nickmatzke — February 21, 2007 @ 1:27 pm
February 21st, 2007 at 2:50 pm
Nick:
Nick, the color of insects may have relevance (to those insects and their survival odds) to their habits or environments, but their color doesn't say anything independent about - contains no information specific to - their environment. I am at a loss as to why you or Mesk would insist so.
For instance, there are robins, bluebirds and goldfinches coming through in waves in my garden (uniformly brown/grey from winter) right now. There is also a significant population (I call it a 'youth gang') of ravens who live on the knob all year. None of these birds' coloration gives an observer (me) any independent information about the environment, mine or theirs.
Eagles and hawks who might prey on bluebirds will see them clearly against the ground - the SKY is sometimes that color, but the ground is not. Any predator could see a goldfinch easily in the air or on the ground, anywhere but on a ripe sunflower - and those won't happen until late July or August, and will last maybe a week at that color intensity. It's also easy to see a raven in the daylight, and mine have no qualms about doing their gang thing (begging food from picnickers or stealing food from hawks) during the day.
A goldfish doesn't provide me with "information" that water is gold. A Luna moth doesn't inform me that the night is light green. This makes no sense.
The fact that the moths are primarily darker these days than they used to be may indeed reflect "information" about the value of the color in their own self-defensive camouflage, if such camouflage is of value to their survival. That may, in addition to past records kept by humans and a good deal of observation, tell us something about selection factors affecting these moths, and the result of that selection on their primary colors. But the moths don't care (they have no ability to change their colors even if they did recognize the problem, which is highly questionable). And the birds don't care (they'll eat whatever moths they can find). Neither the moths nor the birds have received any "information" about the environment by observing the color of moth wings.
And while I do remember when much of western and central Pennsylvania were a uniform color of coal-dust gray, the information I gleaned from that is that coal dust was polluting the environment. I do not recall that birds, flowers, bees or butterflies turned coal-dust gray upon "information" - the obvious - that coal dust was polluting the environment.
We can count growth rings in ancient trees to see where there were periods of drought during their lifetimes. But the fact that we have devised ways of interpreting such evidence *as* information about the environment does not mean the tree changed its physical nature based on encoded information about the environment in its genes. It just grew slower when it had less water. Sometimes the sloppy pronouncements of interpretors (in this case, you and Mesk) is way more anthropocentric than any creationist I ever met.
Unless you wish to support some sort of neo-Lamarckism, the results of 'random' mutation and resulting selection tell us nothing about environments. They just tell us which variants survived, then project our own just-so stories about "why" onto what is given. You cannot read a particular gene's code or the resulting aa sequence in its protein product to determine that "the environment turned black." The information simply is not there.
Comment by Joy — February 21, 2007 @ 2:50 pm
February 21st, 2007 at 5:34 pm
Joy, by your argument, the genome contains no information. I doubt the creationists would like that.
Comment by Nick Matzke — February 21, 2007 @ 5:34 pm
February 21st, 2007 at 6:29 pm
Joy,
Simple questions:
1. Do you agree that the forms of organisms (and the genomes that encode them) closely match (that is, are adapted to) their environment?
2. Do you agree that selection can increase the match between an organism's form and its environment?
If you answer yes and yes, you agree that selection can transfer information about an environment into the genome, and thus increase genetic information.
Your major criticism seems to rely with the notion that this information doesn't exist if it's not easily interpretable by humans (e.g. the fact that colouration doesn't always match environmental colour). But this is completely irrelevant: whether humans can understand it or not, organisms still contain information about their environment because they are adapted to it. And when selection increases adaptation, it also increases that information.
Comment by Mesk — February 21, 2007 @ 6:29 pm
February 21st, 2007 at 6:46 pm
Nick, and Mesk:
In what way was the "information" you are proposing was "created" by evolution in the moths NOT already coded in the moth genome prior to changes in the environment? In what way is the mere statistical change in manifestation of already existing information tantamount to the creation of new or novel information? And in what way can this statistical phenomenon be said to be an increase in organization, when there is no new organization being created?
Comment by Douglas — February 21, 2007 @ 6:46 pm
February 21st, 2007 at 6:50 pm
Joy wrote:
Good grief, Joy, do you really think Nick is talking about moths and birds consciously thinking about moth colors?
The information is in the moth genome, just as the information about a dolphin's watery environment is present in its genome (in the form of genes coding for sleek skin, streamlined shape, fins and flukes, sonar, etc.). Have you ever seen all of those same characteristics present in a terrestrial mammal? If you had never seen a dolphin before, wouldn't you nevertheless be able to deduce its aquatic habitat, simply from seeing a specimen?
Comment by keiths — February 21, 2007 @ 6:50 pm
February 21st, 2007 at 6:59 pm
Nick:
I didn't say that. I am saying that the genome carries no information about the exterior environment (day or night, winter or summer, high or low, warm or cold, blue or orange) in which the organism lives its life. An organism's genome carries information for construction and maintenance of its many systems and subsystems.
The gene-phene map thing was discredited long ago, yet here you are making the even more outrageous claim of a gene-exterior environment and way-of-life map.
A toad can be dark brown. A person can be dark brown. We can presume there are genes for dark brown in the toad's genome and the human's genome. What information does this DNA sequence impart to you about the exterior living conditions of toads and humans?
Comment by Joy — February 21, 2007 @ 6:59 pm
February 21st, 2007 at 7:11 pm
The dolphin response to Joy is apt. There is a heck of a lot of information about the dolphin's environment in the dolphin's genome. It is perhaps arguable that one small trait taken in isolation (like color) sometimes might not be enough to allow one to deduce details of the environment — but this argument breaks down once you look at a large number of traits which are all adapted to the same specific environment.
What are we arguing about again? Creationists ignorantly claim that evolution can't create new information. Joy seems to be defending this position. Even if Joy's argument about genomes not having information about the environment were right, she still hasn't dealt with my main argument, which is that the origin of new genes with new functions is a common and well-understood process, with thorough review articles published in places like Nature Reviews Genetics (e.g. the Long et al. paper).
Clearly, the simple and correct stance to take is that the creationists are just wrong on this one, and that scientific literature does exist which Michael Egnor claimed doesn't exist. What say you, Joy, why not just agree with me, and let's move on to something else?
Comment by Nick Matzke — February 21, 2007 @ 7:11 pm
February 21st, 2007 at 7:12 pm
keiths:
You're addressing a question you made up, and not addressing the assertion Nick and Mesk have made. They don't need to "see" the environment. They tell me they can "read" information about the environment in the genome.
Do let us know when you can deduce the shape of some anonymous organism by "reading" its genes. Until then, you rely on your eyes to "see" shapes and colors and contrasts. Just like I do, just like the moths do, and just like the birds hunting for the moths do. What you see in your life is NOT encoded as information in your genome, and Nick can't "read" it there.
Comment by Joy — February 21, 2007 @ 7:12 pm
February 21st, 2007 at 7:47 pm
Nick,
I know it's helpful to avoid addressing Creationist points which refute your claims, but could you please try to make an exception in my case? I really don't want to have to repeate my points a third time.
Comment by Douglas — February 21, 2007 @ 7:47 pm
February 21st, 2007 at 8:34 pm
Douglas,
What's your definition of "information" Why don't the 20+ examples of new genes in the Nature Reviews Genetics count as the evolution of new information? If you definition excludes the peppered moth melanism mutation, fine, but what excludes all of those new genes? If new genes aren't new information, what is?
Nick
Comment by Nick Matzke — February 21, 2007 @ 8:34 pm
February 21st, 2007 at 8:49 pm
Those systems reflect the organism's environment, because its ancestors were selected to live in that environment. As such, the genome (and the heritable epigenome) contains almost all of the information required for the organism to survive in that environment.
C'mon, Joy, this is obvious. A moth's genome encodes information about what it takes to do moth things. A fox's genome encodes information about foxy activities. This is information about the environment.
The notion of one-gene-one-trait is dead and buried, but the notion that the genome is largely responsible for determining phenotype is unscathed (just more complicated).
An organism's genome largely determines its phenotype. That phenotype has been selected for a particular environment. Thus, the genome contains information about the environment.
Let me be clear here: we're talking about populations over evolutionary time, not individuals over single generations. Certainly an individual brown toad might be sitting in an environment that is unsuitable for brown colouration, but he won't be for long.
Before we get too bogged down in the details, Joy, let me ask you again these two questions:
If we can't agree on the answers to these two questions we probably can't continue very far with this discussion, so let's clarify that now.
Comment by Mesk — February 21, 2007 @ 8:49 pm
February 21st, 2007 at 9:14 pm
Joy wrote:
Joy,
It's true that I can't derive the shape of an organism from its genes. It's also true that if I give you the sequence of 1's and 0's on your computer's hard drive, you won't be able to predict its behavior under novel conditions.
Does that mean that there's no information on your hard drive or in the genome? Of course not. In both cases the information is there, even if you or I are unable to interpret it.
Comment by keiths — February 21, 2007 @ 9:14 pm
February 22nd, 2007 at 2:24 am
Nick,
Is this all you can do?
Care to explain how this "survey for young genes in species of the Drosophila melanogaster subgroup by using fluorescence in situ hybridization" supports your Blind Watchmaker religion?
Comment by inunison — February 22, 2007 @ 2:24 am
February 22nd, 2007 at 2:55 am
Nick would you kindly repond to my post dated February 20, 2007 @ 10:52 pm. I think you are misrepresenting Egnor but I may be wrong
Perhaps you could also respond to Egnors challenge while you are at it.
Vivid
Comment by Vividbleau — February 22, 2007 @ 2:55 am
February 22nd, 2007 at 6:07 am
Hi Vivid,
You asked Nick to respond to Egnor's challenge, which is:
Motoo Kimura did just that, in 1961. The following is from the summary section of the paper:
I think this satisfies Egnor's 'challenge'.
Reference:
Kimura M (1961). Natural selection as the process of accumulating genetic information in adaptive evolution. Genetical Research 2: 127-140.
Comment by KC — February 22, 2007 @ 6:07 am
February 22nd, 2007 at 10:32 am
Mesk:
You told us that this particular dark form of the moth species examined encoded the 'information' that its environment is dark. I questioned that assertion, maintaining that the color of the adult form of the insect tells you nothing about the environment. It just tells you (if you could read it) that the adult moth has dark wings.
Dark wings might serve any number of survival strategies for the moth. It could be a night-flyer, its darkness disguising it from night-hunting birds. It could be a shadow-dweller, its darkness disguising it from predators. It could be a scale-reproducer, laying eggs on diseased plants where there will be lots of food for the kiddies. Or its larval form could be dark for any number of reasons a caterpillar might need to be dark, and the adult form ends up with the leftovers.
Yet you tell me these dark moths are dark because of coal dust pollution, and that is written into their genome. That is positively Lamarckian… if it were true, but it's not. I have yellow moths and white moths and blue moths and day-glo green moths around here. I can assure you that my world is not yellow, blue, white or day-glo green. You cannot read the color of the environment from the genes encoding coloration of moth wings.
Some are, some less so. Depends on how one views "closely match" and what the environment actually is. Which cannot be read from gene sequences. You seem to be laboring under the misapprehension that we have "ideal" genomes for any and all species of life on this planet, therefore know how to read a "closely match" from the sequences. This is not so. We determine most matches to conditions from observing form and function in the environments. Conversely, we determine aberrations the same way.
Of course I do. But I don't get that information by reading genomes, and neither do you.
Comment by Joy — February 22, 2007 @ 10:32 am
February 22nd, 2007 at 2:58 pm
No KC that won't do. This is why:
Better luck next time.
Comment by inunison — February 22, 2007 @ 2:58 pm
February 22nd, 2007 at 5:01 pm
All information-theoretic inequalities (such as "new" information/information) are expressed in an epistmic/ontic distinction. (Reflecting the fundamental "philosophical" difference of opinion amongst probability theorists. (Representing something more than that?)
Like his cousin in the Garden, Dembski is "subtle," "cunning" (And up to no good! LOL); he's led us into the trap (Of our making!) of confusing and eliding the difference. What is "new" to you, and me, and everyone else… is not necessariy "new."
I sincerely wish you all luck, KC, because this problem has vexed me to no end! (And even though I am a "neutralist," I don't think much of Kimura's solution.)
Comment by Rock — February 22, 2007 @ 5:01 pm
February 22nd, 2007 at 5:54 pm
Well, it's easy if I can choose the units.
Let's look at the Long et al. paper which I have been citing continuously throughout this thread, but which none of you oh-so-sure-of-yourselves ID guys have even tried to read and rebut.
Table 2 contains 22 examples of new genes of known age. Just for the genus Drosophila, 4 new genes are listed that are known to have arisen in the past 3 million years. This is a bare minimum, since the paper is from 2003, only a few species of Drosophila have had their genomes studied, and within that study only a few of the examples of new genes will have been discovered, analyzed, and published.
Just to make it sporting, let's say that 4 different species of Drosophila produced these 4 genes (probably not true, I haven't checked). This gives us a rate of 1 new gene per species per 3 million years (as a bare minimum).
"That's pretty slow!", you say, forgetting that this was a bare minimum. Now consider that this planet has more than 2 million species and about 3.5 billion years to work with. Even if the average number of lineages/species was not 2 million but, say, only 100,000, that gives us a potential for 116,000,000 new genes. For all we know this is more distinct genes (excluding the genes that are "the same", e.g. the genes with similar sequence and same function in two different organisms) than actually exist on the planet right now.
(The reality is that genes are regularly lost as well as gained — it's all rather like speciation and extinction actually — but Egnor foolishly, incredibly, jaw-droppingly-ignorantly thought that the origin of new genetic information was some kind of huge problem for evolution. Time for the creationists to give up on this one.)
Comment by nickmatzke — February 22, 2007 @ 5:54 pm
February 22nd, 2007 at 6:09 pm
.)
Nick,
Thanks for your reply. So that I am clear you are saying that the new information that NDE can generate is 116,000,000 new genes. Now where would one go and find the peer review references that list this number?
Nick I think you are mistating Egnors position. I dont think Egnor thinks that NDE cannot produce new information it is the amount of info that it can produce that he is looking for. Thats my take given a fair reading of Egnor.
Is Egnor a creationist?
Vivid
Comment by Vividbleau — February 22, 2007 @ 6:09 pm
February 22nd, 2007 at 6:24 pm
Im not 'oh so sure" but I am open to it and not afraid of looking at the evidence. I recognize that all scientific theories are subject to criticism and change. You on the other hand are a dogmatist, a Darwinian fundamentalist and not open to any scrutinny regarding your pet theory. Thats just my opinion based on my observation. I am sure your a good guy and are a person of integrity just as I am sure that Christin fundies are also. But the nature of fundies is that they are just scared because when you challenge ones world view things can get a bit emotional. Thats understandable.
Vivid
Comment by Vividbleau — February 22, 2007 @ 6:24 pm
February 22nd, 2007 at 11:15 pm
Inunison, your parroting of Don Batten's review of Walter Remine (without properly citing him, I might add), doesn't impress me in the slightest. For example, how do comments on neutral theory have any bearing on Kimura's reasoning here, since we are talking about the substitution of alleles by natural selection, not drift. Surely you haven't already forgotten that both Kimura's paper and Egnor's 'challenge' concern natural selection's ability to add information to the genome.
As for pleitropy so what? If the rate of informational increase can be shown to be directly proportional to the substitutional load (and Kimura makes the argument that it can), then we are concerned with the changes in the allele's frequency, not the effects of its expression. Furthermore, you will you recall Haldane's cost of substitution (which Kimura calls the 'substitutional load") is dependent on the initial frequency of the allele, not the selection intensity. So, even if the gene has pleitropic effects, that isn't a factor when making the informational calculation.
Regarding polygenic effects, sorry, but no cigar. Kimura is considering the simplest situation here. Adding polygenic effects to the calculations does not change the fact that information is increasing in the in the genome, it just makes the computations more complex.
You and I can discuss the merits of Kimura's reasoning, if you like. But Egnor's challenge was met, which was the point.
Comment by KC — February 22, 2007 @ 11:15 pm
February 22nd, 2007 at 11:39 pm
Hey Rock,
To be honest, I'm not fond of the information theory-type solutions either, and I think for the same reasons you are. But Egnor was so insistent on getting a set of numbers that Kimura's paper seemed as good as any, in my opinion. But answering Egnor's challenge doesn't even require something as elegant as Kimura's paper. I prefer straightforward reasoning, preferably backed with some empirical juice (so I can avoid all those bigass equations). We know from experimental data, for example, that random mutations in genes that code for promiscuous proteins can produce novel functions. My spidey-sense tells me that is an increase in genetic information. The same goes for gene duplication followed by subsequent divergence in the sequences via mutation. I certainly don't need any steenking equations to tell me Egnor's basic assertion is bunk.
Comment by KC — February 22, 2007 @ 11:39 pm
February 23rd, 2007 at 2:15 am
Hi KC,
Nice to correspond with you again. I hope all has been going well for you and your family.
What do you think Egnors basis assumption is?
Vivid
Comment by Vividbleau — February 23, 2007 @ 2:15 am
February 23rd, 2007 at 4:59 am
Um, you saw the math right there. And that's the bare minimum potential. (You realize the whole human genome has only 30,000 genes, right?)
Scientists wouldn't bother to publish something like this because it is obvious to anyone who is vaguely familiar with the relevant science that there is no meaningful "upper limit" to the amount of information evolution can generate. Once it is established that evolution can produce new genes reasonably frequently, any attempt to say that "evolution can only produce X amount of information" is totally hopeless, because X+1 more gene is trivial to produce.
Oh, c'mon, he was clearly arguing there was some very low limit and that this was some huge problem for evolution — he probably had Dembski's 150 bits or something in mind.
I don't actually know offhand, but I'm sure he is. The no-new-information argument is pretty much unique to creationists.
Comment by nickmatzke — February 23, 2007 @ 4:59 am
February 23rd, 2007 at 6:55 am
Hi Vivid,
Egnor's basic assertion (not assumption) is that ther is no evidence that new information can arise in the genome via RM&NS. That's why he keeps asking this question over and over:
Kimura's paper shows that it can, taking a population genetics approach. I also pointed out to Rock examples where mutations can produce novel functions in proteins, which to me points squarely to an increase in genetic information by any objective measure, IMHO. So I think Egnor's assertion is bunk.
I hope all is well with your family as well.
Comment by KC — February 23, 2007 @ 6:55 am
February 23rd, 2007 at 2:51 pm
Nick:
It isn't true. The 4 genes you are referring to are from different branches of species: one from African flies and the other three from D melanogaster. The lineage structure would not allow you to compute them this way(4/4=1).
Nonetheless, I don't think that these kinds of computations can be generalized anyway, I am not sure if the derived number means anything. We only have good data from Drosophila and other organisms (e.g. mammals), with regard to how many we can call a species. Another thing is, you would think from studying the suite of wnt genes in humans and Drosophila that it followed a gradualistic process of a rise in complexity. You would think that cnidarians have one, nematodes and insects about 4-5 and vertebrates 12. New genes arise all the time right? Gene duplications and increase of complexity go hand in hand.
However, the data shows the complete opposite, the complete set of wnt genes in the urbilaterians. It points to a rather different evolutionary scenario. Based on the clear clustering of the Wnt gene families it is highly unlikely that a single Wnt gene independently expanded in the cnidarian and vertebrate lineages. The system was optimized by fine tuning, but also by gene loss. There's also the weird facet that hox genes are only rudimentary present in cnidarians, making the complexity of wnts even more fascinating.
Comment by Guts — February 23, 2007 @ 2:51 pm
February 23rd, 2007 at 6:00 pm
So, multiply my estimate by 3, since D. melanogaster is undoubtedly where we have the most thorough information. So, 1 new gene per million years per species is definitely within the capacity of evolution — contra Egnor.
You are picking and choosing your data here — as you note, the Hox genes do have exactly the pattern you request. All that the wnt data indicate is that they arose before the common ancestor of the metazoa (well, most of them, apparently the sponge genome is missing one). But even fungi have one wnt gene.
The next obvious place to look is the choanoflagellate genome — it wouldn't be at all surprising if it perserves a wnt collection intermediate between fungi and metazoans. (It looks like the choanoflagellate genome should be published pretty soon.)
Comment by Nick Matzke — February 23, 2007 @ 6:00 pm
February 23rd, 2007 at 6:42 pm
Nick:
Why would I multiply it by 3? Wouldn't it be 3 divided by 3 million years = 1 per species per million years if you're just looking at data from D. melanogaster (obviously it's much higher than this).
Nick:
Actually, the hox cluster and code studied in this paper appear to be pretty ancient as well. Sponges (non bilaterians) might have one wnt gene, and cnidarians (i would argue are bilaterians) might have 9, but when did 'bilaterianism' occur? And how many genes did this critter have? The molecular complexity of nematostella does not have obvious morphological "outputs". These animals have been thought to be "simple". What have they been doing with all these genes all these years? (Rhetorical question and just thinking outloud, does not require an answer).
Comment by Guts — February 23, 2007 @ 6:42 pm
February 23rd, 2007 at 6:46 pm
The guy truly doesn't know what he's talking about when it comes to evolutionary theory. So having his name on the Dissenters from Darwininsm list is something the DI should probably not want made public. Oops. Too late.
To the contrary. Egnor is alluding to a predictive possibility for ID that would contrast with MET. That's the type of thing critics have been asking for. A particular biological system needs to be specified as well as a means of determining pathways and dead ends to pathways. He's got his finger on the relationship between IC systems and selection.
Comment by Bradford — February 23, 2007 @ 6:46 pm
February 23rd, 2007 at 6:50 pm
Oh really? Since when does evolutionary theory state that every step must have a selective advantage, 'no exceptions'?
Comment by KC — February 23, 2007 @ 6:50 pm
February 23rd, 2007 at 6:51 pm
That's what I said. My first guesstimate was 1 gene per species per 3 million years, or 1/3 gene per species per my. Multiple by 3 = 1 gene/species/my.
Comment by Nick Matzke — February 23, 2007 @ 6:51 pm
February 23rd, 2007 at 8:37 pm
So you have a change that is fixed in the genome with no selective value?
Comment by Bradford — February 23, 2007 @ 8:37 pm
February 23rd, 2007 at 8:41 pm
Egnor clearly was not referencing nucleotide changes that do not change a protein.
Comment by Bradford — February 23, 2007 @ 8:41 pm
February 23rd, 2007 at 8:57 pm
Does this reduce your previous number of 116,000,000. genes?
Vivid
Comment by Vividbleau — February 23, 2007 @ 8:57 pm
February 23rd, 2007 at 9:08 pm
KC,
Thanks for your response. Then you would anwswer Egnor that this is at least the minimum amount of information that Darwinian evoution can produce?
I dont think this is a fair reading of Egnor"s position but we see want we want to see ( myself included).
Vivid
Comment by Vividbleau — February 23, 2007 @ 9:08 pm
February 23rd, 2007 at 11:01 pm
Sure, neutral substitutions fix as well - it just takes longer. A new neutral mutation will fix with a probability of 1/(2Ne), where Ne is the effective population size, and it will take 4Ne generations on average to do so.
In small populations even mildly deleterious mutations can be fixed, albeit with a much lower probability.
KC's absolutely right - the notion that only selectively advantageous mutations can fix displays a lack of understanding of basic evolutionary theory.
Comment by Mesk — February 23, 2007 @ 11:01 pm
February 23rd, 2007 at 11:48 pm
Mesk, KC was criticizing Egnor and if he wants to do that it is incumbet to get Egnor's comments right or become the latest paraspinner. Egnor is questioning the evolution of non-neutral events. He proposes a general test prediction based on it. That's what anti-IDers have been calling for. He used the term steps, which is a little too vague to suit me, but interpreting this as meaning a nucleotide change that retains the same aa while thinking this requires selection is extreme. Incidentally I did write in a previous post:
Egnor clearly was not referencing nucleotide changes that do not change a protein.
A series of mutations, that create a new function and the multiple proteins composing it, should correlate to a series of selective changes. If there are no pathways making this possible, the implications are clear.
Comment by Bradford — February 23, 2007 @ 11:48 pm
February 24th, 2007 at 12:03 am
BTW, I agree with this and think the accumulation of such mutations, over time, can be a contributing factor to extinction with some species. The reaction to Egnor's comment reveals just how vague and poorly understood are most evolutionary pathways. Explanations that encompass virtually every type of change and few specifics lose instructional value.
Comment by Bradford — February 24, 2007 @ 12:03 am
February 24th, 2007 at 12:38 am
Bradford,
Synonymous substitutions (those that don't change protein sequence) are not the only neutral mutations. Mutations that do alter the protein sequence can also be neutral if they don't affect protein folding or function, as indeed can changes that alter expression patterns so long as the gene is still expressed where it needs to be. These mutations allow populations to drift through phenotype space, and to occasionally stumble on highly beneficial locations.
Obviously IC protein complexes don't just build themselves by drift (i.e. randomly) - selection is heavily involved. But drift can also be crucial. For instance, take a process where proteins A and B perform a function, and C is beneficial (but not essential) to this process. Over time, mutations in A and B may make them dependent on C (since C is always present in the cell, such mutations are functionally neutral). This has no marked effect on phenotype, but A, B and C now form an IC complex, such that the removal of any of them destroys the function.
KC isn't attacking a strawman; Egnor stated:
And he is simply wrong; many, if not most 'steps' in molecular evolution are in fact functionally neutral at the time they occur. This has been known at least since the 1980s, so Egnor has no excuse.
And when you say:
You are equally wrong - many of the changes that went into building this complex were neutral at the time, and became functionally relevant only after the fact.
Your point is well taken, and I agree with the statement that most evolutionary pathways remain poorly characterised. There is much work to be done in evolutionary biology, both theoretically and experimentally.
However, regardless of the uncertainties that remain in the field of evolutionary biology, criticisms of evolution that ignore major forces known to influence evolutionary change are simply misguided, and should be taken to task.
Comment by Mesk — February 24, 2007 @ 12:38 am
February 24th, 2007 at 1:09 am
Mesk, significant events are always accompanied by neutral changes. Stipulate the obvious. KC wrote: "So having his (Egnor's) name on the Dissenters from Darwininsm list is something the DI should probably not want made public. Oops. Too late. This is the typical childish potshot that is so common on your side of the aisle. I once engaged an opponent in a discussion about the evolution of the pyruvate dehydrogenase complex and did not once mention synonymous substitutions. The other individual although of a different view did not stop and say "look you have not mentioned blah, blah blah. You must be ignorant of evolutionary theory and surely your name would not belong on any list… Frankly, the point is a needed distraction from the real problem which is not neutral mutations but nailing down pathways that have an inkling of detail. As long as vague descriptions suffice for intelligible pathways arrogance will serve as a useful substitute for real explanations.
Comment by Bradford — February 24, 2007 @ 1:09 am
February 24th, 2007 at 1:18 am
This remark would be significant if you were able to point out the non-functionally neutral steps. Of course that gets to the real issue. The actual events that had immediate causal significance in rendering a function are unidentifiable. This is kept from glare of the spotlight when it should be front and center.
Comment by Bradford — February 24, 2007 @ 1:18 am
February 24th, 2007 at 3:50 am
Multiply by three (when we switch to using just Drosophila melanogaster as the measurement, because it had 3 new genes all by itself in just 3 million years), not that it matters. If we want to get picky, Drosophila has a small genome and small genomes likely give birth to fewer new genes than large genomes, so again this is an underestimate of the capacity of evolution.
Comment by nickmatzke — February 24, 2007 @ 3:50 am
February 24th, 2007 at 8:02 am
I wrote:
Bradford replied:
Yes. There can even be steps in an adaptive pathway in which fitness is lost along the way to the peak. Evolutionary theory doesn't forbid such a path, and there is no theoretical reason why it should. And there is empirical evidence that such paths occur. A recent paper talks about them (which I posted at the Time site, under my real name, Dave Wisker):
Poelwijk FJ, DJ Kriviet, DM Weinreich and SJ Tans (2007). Empirical fitness landscapes reveal accessible evolutionary paths. Nature 445: 383-386.
From the paper (my emphasis):
But the fact is, the adaptation (antibiotic resistance) was achieved in those cases. So Egnor has it completely wrong when he insists every step must have a selective advantage, "no exceptions". In fact, it shows that he truly doesn't understand what modern evolutionary theory says, and if he is signing the list based on such a poor understanding of the subject, then nobody at the DI (or here, for that matter) should be glad he's one of the group.
Comment by KC — February 24, 2007 @ 8:02 am
February 24th, 2007 at 11:43 am
Egnor makes one very telling point. One can cite synonymous substitutions and deleterious mutations and make claims (not disputed) that they were part of pathways. Weather forecasters make references to temperature, areas of high and low pressure, humidity and wind flow and direction. In that way they are similar to those who note the different types of changes that can be part of a pathway. However weather forecasters also attach specific numbers to their variables and by the time they are finished a listener can get a very good idea as to what the weather will be like that day.
Contrast this with evolutionary pathways to a number of complexes I could cite. Sure, you are able to rattle off different types of mutations that are no doubt part of such pathways. But where is the corresponding specificity that would enable a reader to get a good grasp of how the events actually unfolded? A lack of real specificity is the more important theme of the controversy. It is more important than the interview of Egnor. More important than the blog reactions. More important than what you or I say about it.
Comment by Bradford — February 24, 2007 @ 11:43 am
February 24th, 2007 at 12:04 pm
Interesting….I ask nick for a specific number with references he gives me 116,000,000 new genes ..no references. Then overnight it seems it changes by a factor of 25%. Sounds to me Nick you have no clue.
KC on the other hand did give me a number and references.
Vivid
Comment by Vividbleau — February 24, 2007 @ 12:04 pm
February 24th, 2007 at 3:43 pm
The basic problem is that gradual evolution via RM&NS has great difficulty with a system with numerous interdependencies (i.e. an IC system). This is a real problem which takes into account - local optima , landscape ruggedness,high fitness peaks, IC configurations, etc - they do not admit evolution by accumulation of small modifications.
If you have an IC system AB, AB is not evolvable by RM&NS. The two systems (A and B) must evolve in parallel and gradulastic evolution cannot easily search combinations of different variants of A and B because not all variants of A will work with all variants of B. For example, in eubacterial flagellins there has to be conservation of domains that mediate inter-subunit interactions for assembly to occur. Despite all these problems , and as KC has mentioned, we still get an adaptation (although the example is not very complex). Not only that but if you have a have a good sized population, the best mutation wins time after time, you can even tell beforehand which of a few mutations will win out. There must be something more complex at play than mere gradual random variation and selection driving adaptation. Natural selection is not omnipotent.
Comment by Guts — February 24, 2007 @ 3:43 pm
February 24th, 2007 at 4:27 pm
Guts writes:
Mutations to promiscuous proteins can evolve such a system this way, since it doesn't matter whether or not the variants work together at first because the core functions of the proteins would be unaffected.
Comment by KC — February 24, 2007 @ 4:27 pm
February 24th, 2007 at 4:40 pm
KC:
Thats not what I saw in the paper you referenced. One of the experimenters concluded that changes to amino acid sequence are immensely context-dependent (i.e. their effect depends extensively on which other mutations are already present, epistatic interactions),and why a only very small number of selectively important trajectories are likely to exist to high-fitness proteins.
Comment by Guts — February 24, 2007 @ 4:40 pm
February 24th, 2007 at 5:35 pm
Guts writes:
The basic idea wasn't in that paper. The one I had in mind was:
Aharoni A, L Gaidukov, O Khersonsky, S M Gould, C Roodveldt and DS Tawfik (2004). The 'evolvability' of promiscuous protein functions. Nature Genetics 37, 73 "“ 76
The authors talk about how mutations to the promiscuous functions could occur without harming the core function, and that with gene duplication and divergence, you could get entirely new proteins. Conceivably, the precursors to your "IC" system could start as promiscuous functions on different proteins, and could acquire variations that are eventually compatible with each other in parallel without having to undergo significant negative selection, since the core functions of each protein remain unaffected. This means it is quite possible to build an "IC" system in a Darwinian fashion.
Comment by KC — February 24, 2007 @ 5:35 pm
February 24th, 2007 at 7:51 pm
KC,
Yes what the paper hypothesizes is in line with what I said. You can have a protein A and a protein B that each evolve gradually because they might have promiscuous functions (evolvability), and then specialize, but AB is not evolvable as a whole, nor are they evolvable one after the other in the same individual, that is because AB is IC. They cannot evolve together gradually because of dependencies acting between each system. "A" can evolve step by step but it would be extremely difficult for protein B to evolve without causing catastrophic fitness decreases by disrupting dependent interactions with A.
What I'm referring to is what this paper paper and the one you referenced calls "reciprocal sign epistasis". Where:
It's when one variable is said to be dependent on another when the effect of changing the variable is dependent on the state of the other. Many variables have to change simulataneously before a higher fitness value can be obtained. I can go a bit deeper but this is enough to chew on. The basic gist of what I'm saying is that IC systems create multiple peaks on a fitness landscape, and "The presence of multiple peaks indicates reciprocal sign epistasis, and may cause severe frustration of evolution".
Comment by Guts — February 24, 2007 @ 7:51 pm
February 24th, 2007 at 9:49 pm
Egnor ask"
KC references Kimura 0.29 bit/generation
Evidently Kimura has demonstrated that RMNS ie trial and error can generate? KC how many bits of information would this equate to over the history of evolution?
I am curious to know because if in fact it has been proven that RMNS can generate enough information for all that we see then the ID argument is DOA.
Vivid
Vivid
Comment by Vividbleau — February 24, 2007 @ 9:49 pm
February 25th, 2007 at 3:43 am
Vividbleau wrote:
Vivid, you yourself quoted Egnor in this thread saying:
Nick is right. Egnor obviously believes that no new information can emerge from RM + NS.
This is, quite frankly, an Egnorant position to take.
Comment by keiths — February 25, 2007 @ 3:43 am
February 25th, 2007 at 3:57 am
.
Surprise surprise Keith agrees with Nick…what a shock (gasp). I still think that a fair reading of Egnor shows it is false to say that Egnor believes that no new information can emerge from RMNS.
Keith please read this communication between Egnor and Lemonick and try taking your idealogical blinders off that cause you to so easily classify ID proponets as ignorant, stupid or dishonest.
Vivid
Comment by Vividbleau — February 25, 2007 @ 3:57 am
February 25th, 2007 at 4:07 am
Vivbleau writes:
Vivid,
Egnor's own words contradict you:
Are you telling us that Egnor didn't mean what he said here, or that you know better than Egnor what Egnor's position is?
Talk about ideological blinders.
Comment by keiths — February 25, 2007 @ 4:07 am
February 25th, 2007 at 4:17 am
Keith I see I will have to hold your hand.
Here Egnor is quite clear of the type of information Egnor is referring to.
Keith do you see the phrase "significant new information" Egnor is not saying that RMNS cannot produce no information his point is can it produce significant new information.
You cannot take this paragraph out of context of what has been said before. Goes to show that quote mining is not relegated to the creationists.
As I said take your blinders off and give Egnor a fair reading.
Vivid
Comment by Vividbleau — February 25, 2007 @ 4:17 am
February 25th, 2007 at 5:01 am
Egnor: In 150 years, Darwinists have failed to provide even rudimentary evidence that significant new information, such as a code or language, can emerge without intelligent agency.
Vivid: Keith do you see the phrase "significant new information" Egnor is not saying that RMNS cannot produce no information his point is can it produce significant new information.
Keiths, when a writer uses a phrase like "significant new information" it is a clear tip-off that he is introducing a homemade term he is entitled to define as he wishes. The definition Egnor had in mind is revealed in the same sentence. It consists of a code or language and the limit on the generation of such is qualified by the phrase "without intelligent agency." Disagree with Egnor if you wish but don't fall into the trap of paraspinning.
Comment by Bradford — February 25, 2007 @ 5:01 am
February 25th, 2007 at 5:26 am
Here is another quote from Egnor:
This quote is interesting on three levels:
1. It shows that Vividbleau and Bradford are wrong about Egnor's position. He clearly doesn't believe that even a single beneficial mutation is possible:
2. He clearly doesn't understand the concept of IC, since he believes that every beneficial mutation is IC. Behe would never make such a claim.
3. He doesn't understand evolution, since he believes that every step in an evolutionary process must confer a selective advantage.
If you guys want to continue backing someone whose position disagrees with yours, who doesn't understand evolution, and who doesn't even understand ID theory, then be my guest. The credibility is yours to squander.
Comment by keiths — February 25, 2007 @ 5:26 am
February 25th, 2007 at 5:33 am
:
Ahh Keith bait and switch
Comment by Vividbleau — February 25, 2007 @ 5:33 am
February 25th, 2007 at 6:38 am
Vivid:
LOL. Care to explain why we should ignore Egnor, but pay attention to you, in figuring out what Egnor believes?
Maybe you should call Egnor up and tell him what he believes.
Comment by keiths — February 25, 2007 @ 6:38 am
February 25th, 2007 at 6:41 am
It was amusing to read Vividbleau's accusation of quotemining, considering that he had just quotemined Nick.
Vividbleau, quoting Nick:
…and then rendering judgment:
Vivid,
Did you really think you could get away with quotemining Nick in the same thread that his comment appears in?
Here's Nick's comment, with the part you omitted in bold:
Kinda undermines your point, doesn't it, Vivid?
Now let's look at your claims:
The number Nick gave you was an extremely conservative lower bound, so of course the exact number 116 million does not appear in the literature.
As Nick said, that number is a bare minimum. Look at all the concessions he made to bias the number in your direction:
1. He counted only the known new genes in Drosophila. Do you really think we've discovered them all?
2. He assumed that each of the four new genes appeared in a different species, so that only one new gene is counted for Drosophila melanogaster over the 3 million year period.
3. He based his calculation on Drosophila, which has a small genome, despite knowing that new genes arise more quickly in larger genomes.
4. He ignored the fact that genes are lost as well as gained.
Despite these concessions, he still came up with a number that was so far from zero as to make Egnor look ridiculous.
As for the change in Nick's number, it came about because Guts helpfully pointed out that 3 of the 4 new genes occurred in Drosophila melanogaster, which means that Nick's number could have been 200% larger (I don't know where you came up with 25%). But as Nick said, in the part of his sentence that you carefully snipped out, it doesn't matter. Whether the number is 116 million or 348 million, it's so far from zero as to devastate Egnor's claims.
I already explained why the 116 million figure does not appear in any references, but the numbers that motivate Nick's calculation come straight from the Long et al. paper, which he cites.
Care to reconsider your assessment, Vivid?
Comment by keiths — February 25, 2007 @ 6:41 am
February 25th, 2007 at 7:17 am
Hi Vivid,
Kimura estimated the increase in information since the beginning of the Cambrian. The figure he came up with was 10^8 bits. Of course, a large part of life's complexity (cellular metabolism, multicellularity, eyes, etc) had already been established by then.
Is 10^8 enough to explain the complexity that we see today, as compared to the Cambrian? I'm not sure. We have to carefully define what we mean by 'complex'. Sure, we have seen a lot of diversity since then, but diversity doesn't directly translate into complexity. However, if anybody is going to say 10^8 bits isn't enough, I'd like to see their calculations.
Comment by KC — February 25, 2007 @ 7:17 am
February 25th, 2007 at 7:31 am
Oh Keith you got your hand caught in the cookie jar and now you want to shift the focus on me. I in no way quote mined Nick. Lets review shall we.
Nick gave a figure of 116,000,000 genes. Guts brought up a few comments and Nick said to Guts
So, multiply my estimate by 3,
I then asked Nick
Does this reduce your previous number of 116,000,000. genes?
Vivid
Nick responded
Multiply by three (when we switch to using just Drosophila melanogaster as the measurement, because it had 3 new genes all by itself in just 3 million years), not that it matters. If we want to get picky, Drosophila has a small genome and small genomes likely give birth to fewer new genes than large genomes, so again this is an underestimate of the capacity of evolution.
Now if I am guilty of anything I am guilty of not understanding what Nick meant. My take on it was at first Nick was multiplying by 4 and now was multiplying by 3 a 25% reduction thus my comment. The rest of Nicks comments were not relevant to my calculation especially since I gave credit to KC referencing Kimura. Try again.
Yes it seems I misunderstood what Nick meant"¦I can admit when I am wrong. Can you?
Lets look at your behavior. You quote mined Egnor then when called on it rather than admit your error you pulled a bait and switch.
WHo are the "you guys" I am not backing Egnor on anything. However when you and your ilk accuse the man of being ignorant, egnorant, ridiculous and basically a crank based on the comments I was referrng to I will stand up for the guy especially as I and bradford have already pointed out is not a fair reading based on the comments we were discusiing not your bait and switch.
Vivid
Comment by Vividbleau — February 25, 2007 @ 7:31 am
February 25th, 2007 at 7:35 am
Hi KC,
How would we compare Kimur's bits to the amount of bits in the human geome. Any idea? Thanks
Vivid
Comment by Vividbleau — February 25, 2007 @ 7:35 am
February 25th, 2007 at 7:50 am
Nick,
In referring me to some other supposed increases in "genetic information via evolution", and implicitly dropping your claim that the statistical variation in percentage of melanin in a moth population is evidence of evolution, you are conceding that I am right, and you are wrong (about the "variation in melanin is evidence of evolution" claim). Therefore, my work here is done (I think), and I will ride off into the sunset, victorious and full of glory.
Comment by Douglas — February 25, 2007 @ 7:50 am
February 25th, 2007 at 8:07 am
Vividbleau claims:
Right. You just accidentally ended the quote at a comma, dropping the final four words of Nick's sentence: "not that it matters." Four words which, purely by accident, just happened to negate the point you were trying to make. Got it.
Let's review:
1. We disagreed on the meaning of Egnor's first comment.
2. I provided a second quote from Egnor which confirmed that my interpretation was correct and yours was wrong.
Therefore:
A. I quotemined Egnor, because I represented his position correctly.
B. I pulled a bait-and-switch, because I supplied a quote which confirmed that I had represented his position correctly.
C. We should go back to using your incorrect interpretation of Egnor's position.
Got it. Makes sense to me.
Vivid, this was amusing for a while, but now it's just turning sad.
Comment by keiths — February 25, 2007 @ 8:07 am
February 25th, 2007 at 8:13 am
Guts,
If you recall, the authors say that, when there is no epistasis, mutations to A have the same fitness effect for different genetic backgrounds (in your case, B). That is what the authors are describing and here is why: fitness of the gene for protein A is tied to the core function, not the promiscous function. The same goes for B. Thus mutations to the promiscuous function can occur without a change to the overall fitness of the gene for the protein. If the "IC" system AB consists of interactions of the promiscuous functions of both proteins, changes can occur in each independently of the other without drastic changes in fitness until the right combination is found for the new system. The fact the two can vary independently without drastically affecting fitness eliminates the multiple peaks. There is one big assumption here, however, that there is no immediate adaptive need for AB due to a deteriorating environment, or other such drastic situation.
Comment by KC — February 25, 2007 @ 8:13 am
February 25th, 2007 at 8:20 am
The point I was trying to make was that Nick had overestimated his number the other words had nothing to do with anything LOL.
To quote mine
I did not take a quote from Nick and suggest that he a) adopted a different position than the position he had taken. I was questioning his number not mining a quote that said he did not agree with this number. Are you this desperate Keith?
Yep
Keep paddling Keith.
Vivid
Comment by Vividbleau — February 25, 2007 @ 8:20 am
February 25th, 2007 at 8:24 am
Vivid,
Kimura noted HJ Muller once estimated the maximum amount of information the human genome could contain. He did it by dividing the total mass of DNA in a human sperm by the mass of one nucleotide. Given 4 kinds of nucleotide pairs, the maximum amount of information in the haploid genome was 8 X 10^9 bits. Therefore, the maximum for the diploid genome was 1.6 X 10^10 bits.
Of course, this figure does not take into account pseudogenes, gene duplication, and other redundancies. And remember the 10^8 figure only applied to increases in information since the Cambrian.
Comment by KC — February 25, 2007 @ 8:24 am
February 25th, 2007 at 8:27 am
So that you do not accuse me of quote mining. Yes you did quote mine and no you did not represent his position correctly.
Vivid
Comment by Vividbleau — February 25, 2007 @ 8:27 am
February 25th, 2007 at 10:33 am
Comment by inunison — February 25, 2007 @ 10:33 am
February 25th, 2007 at 1:05 pm
Hi Nick,
I'm late to the party (as usual). Can you provide the complete reference? And how many of the 20+ examples were dependent on gene duplication?
Comment by MikeGene — February 25, 2007 @ 1:05 pm
February 25th, 2007 at 1:25 pm
Nick Matzke, "Why don't the 20+ examples of new genes in the Nature Reviews Genetics count as the evolution of new information?"
I am also quite interested in your 20+ examples. What evidence is there that these were generated by natural processes? Either there is statistical support for their arrival by natural processes or I will see them as evidence for agency.
Comment by bFast — February 25, 2007 @ 1:25 pm
February 25th, 2007 at 5:20 pm
Hi Mike,
Here is the paper I keep bringing up:
Long M, Betran E, Thornton K, Wang W. (2003). The origin of new genes: glimpses from the young and old. Nature Reviews Genetics. 4(11):865-75.
It is free online in various places.
Table 2 lists 22 examples of new genes that are fairly evolutionarily recent and lists references for each. The table also lists the various mechanisms — duplication is usually a part but never the whole story (because merely having a duplication does not produce a "new" gene — additional changes have to occur for it to become something that geneticists would give a new name to).
Table 1 lists all the various mutational mechanisms that are known to play a role in generating new genes.
It's a quite handy paper — I bring it up every time the "no new information" bafflegab is trotted out. (E.g., the PT critique of Stephen Meyer's 2004 paper entitled "The Origin of Biological Information…"; it is even cited in the Kitzmiller decision, along with other work. Egnor, on the other hand, called it "just-so stories.")
The only major limitation in the paper is that it is focused on eukaryotes and ignores prokaryotes; it would be nice to have a similar review for prokaryotes but I haven't found one.
When I am really feeling snarky I point out that it is just one of dozens of papers that Manyuan Long has authored on the origin of new genes.
PS: To Vivid and others, regarding what Egnor claimed — no, he wasn't talking about only the origin of life or the origin of the DNA/protein code. Here is a quote from the Time magazine thread:
Eventually, after getting called on his foolishness by many people with access to the papers like the one I cited, Egnor switched from boldly requesting hard, quantifiable answers to pretending that his questions had been unanswerable rhetoric. From his latest post:
My latest response to Egnor's last reply is over here.
Comment by nickmatzke — February 25, 2007 @ 5:20 pm
February 25th, 2007 at 5:23 pm
Nick,
Excellent. Thanks.
Comment by MikeGene — February 25, 2007 @ 5:23 pm
February 25th, 2007 at 6:11 pm
Well, Vivid, looks like Egnor's question was "rhetorical", despite Kimura's direct answer to it… he wasn't interested in any answer, apparently. Somebody did cite Kimura's paper to him over at the Time blog, which he never acknowledged, or even challenged. Nice.
Comment by KC — February 25, 2007 @ 6:11 pm
February 25th, 2007 at 6:36 pm
Nick, interesting paper. I haven't properly read it yet, just skimmed it. However, I was intrigued that man has about 100 (1%) genes that "have no similarity with the genes of other animals." (p.7) As the processes that I have read about so far in this paper would show a similarity between new genes and their originating genes, especially in light of Haldane's dilemma, I find this number high, rather than "only" as the other describes it.
I wonder what the code similarity between Windows XP and Vista is. I bet its above 99.9%
Comment by bFast — February 25, 2007 @ 6:36 pm
February 26th, 2007 at 1:46 pm
KC wrote:
I don't think this has been shown empirically with protein-protein interactions (AFAIK) and gene duplication is really a large nonrandom change. IC systems have components that exihibit this kind of epistasis, they exhibit numerous interdependencies. Protein interactions aren't easily generated , it's the shape of the protein, the position of active domains, etc that determines its functional interface with other proteins. Epistatic interactions are widespread in nature, and there has been some studies that show that the type of mutation you are referring to might not really make any difference anyway (here). This is why I don't think incremental evolutionary mechanisms can generate large IC systems. (of course by can and can't I simply mean in terms of difficulty, not impossibility.)
I think this line of thought is compatible with what we actually see in nature. Take the Rag machine for example. The Rag machine of the adaptive immune system is irreducibly complex, Rag1 cannot work without Rag2. I think it is significant that the line of thought is that it arrived via horizontal gene transfer, that Rag1 arrived via horizontal gene transfer, and RAG2 emerged after recruitment of the Transib transposase as a protein that was not encoded by the ancestral Transib (AFAIK). I think this is an example of an IC system that arose non-incrementally (because it can't arise incrementally).
Comment by Guts — February 26, 2007 @ 1:46 pm
February 26th, 2007 at 6:14 pm
Yes, it is too high, as the authors would have known if they had skimmed the literature on these genes subsequent to the publication of the human genome sequence in 2001. In the HGP publication, the authors claimed that 223 genes showed no similarity to genes in other eukaryotes, and thus may have been acquired by horizontal gene transfer from prokaryotes. This rather sensational claim was fairly definitively rebutted the same year, in this paper (also see a reasonable lay description here). Essentially what the second paper showed was that almost all of the alleged examples of bacteria to human transfer were in fact artefacts, due to the use of a small number of other eukaryote sequences for comparison. When the authors drew on a larger sample of organisms they were left with only 40 genes, many of which were likely to disappear with further eukaryote genome sequences, with the remainder probably explained by gene loss or rapid sequence divergence in non-human lineages.
I'm pretty sure there was a follow-up paper some time back that further destroyed the claim of microbe-human gene transfer using phylogenetic analysis, but I can't seem to find it today.
I'll take you up on that - I suspect it's below 90%, but I can't find much comparative information on the web (and of course direct comparisons are impossible, given that the source codes are proprietary). Are there any software experts in the audience who can comment?
Comment by Mesk — February 26, 2007 @ 6:14 pm
February 26th, 2007 at 10:55 pm
Hi KC,
I went to the Time blog and did not see any reference to Kimura. I looked for it but the blog as of the 25th is quite long so maybe I just missed it.
Vivid
Comment by Vividbleau — February 26, 2007 @ 10:55 pm
February 27th, 2007 at 6:19 am
Vivid, here is the first one.
I posted it again later:
Comment by KC — February 27, 2007 @ 6:19 am
February 28th, 2007 at 11:21 pm
Guts writes:
I'm not talking about gene duplication. I'm talking about coevolution of promiscous protein functions. Gene duplication may play a part later in creating a specific protein, but it isn't a necessary precursor to the initial development of the interaction.
Your last reference was talking about redundancies (as in gene duplications). Since I'm not talking about gene duplication, it's irrelevant.
Comment by KC — February 28, 2007 @ 11:21 pm
March 1st, 2007 at 12:48 pm
KC:
Yeah but I'm talking about IC systems.
KC:
You were talking about how different variants of A and B can sample different types of interactions via mutations because it didn't matter whether they worked. What the study (and many like it) shows is that this kind of mutational search is as good as "hill climbing" algorithms. Proteins can evolve new functions because they have inherent flexibility in plasticity residues for future benefit, but I don't think you can get an IC system from accumulation of small random variations.
Comment by Guts — March 1, 2007 @ 12:48 pm
March 1st, 2007 at 6:15 pm
Of course you can. I stated above:
I've also noted in another thread recently that many substitutions that increase the dependence of A and B on C are likely to be actively selectively favoured, since substitutions that increase the affinity between the proteins will often boost the functional effects of C.
IC systems of arbitrary complexity could build up in this way over time: accessory proteins appear that aid the function of the complex, and small random variations occur over time that merge these proteins ever more tightly into the complex. Eventually you have a system in which many components are so tightly enmeshed that each is indispensable.
Comment by Mesk — March 1, 2007 @ 6:15 pm
March 1st, 2007 at 7:12 pm
Mesk,
As I already noted, there are IC systems that are not amenable to that kind of small variation, because they require many genetic sites to change simultaneously. In other words, C may not be able to evolve without disrupting these interdependencies with AB (reciprocal sign epistasis). Changes to amino acid sequence are immensely context-dependent. The mechanism you bring up can work where interdependencies are either weak or few in number.
Comment by Guts — March 1, 2007 @ 7:12 pm
March 1st, 2007 at 8:21 pm
Guts,
Sorry, I lost track of the thread and forgot the conversation had moved on.
Comment by Mesk — March 1, 2007 @ 8:21 pm
March 2nd, 2007 at 12:25 am
Guts, you wrote,
That raises several interesting questions:
1) The link to "Protein interactions aren't easily generated" is a link to you stating that "I don't think that it is necessarily true that protein-protein interactions are generated simply," followed by your linking to a paper that has nothing whatsoever to do with protein-protein interactions. What were you trying to convey in both cases? Neither link makes any sense to me. How did you get from thinking that they aren't easily generated to knowing that they aren't easily generated?
2) If it is difficult to generate protein-protein interactions, wouldn't you predict that most proteins should be very soluble in physiological ionic conditions? Is that the case, even for random sequences?
3) Since you'd probably try to argue that interactions between random proteins aren't specific, are virtually all protein-protein interactions in biology specific or merely selective? Which would you predict from a hypothesis of intelligent design?
4) If I replaced a bacteriophage protein, required for binding to a host protein allowing infection, with a random sequence, how many orders of magnitude improvement of phage infectivity would you predict that mutation and selection would produce in a few rounds of infection?
Comment by genomic — March 2, 2007 @ 12:25 am
March 2nd, 2007 at 4:51 am
I would guess that the selective value of proteins is largely determined by specific protein properties enabling interactions between them.
I would imagine the improvement would be dramatic but would hasten to point out the limited scope of this example. What if the analysis instead focused on a function involving a score of proteins and improvement was linked to changes in multiple proteins?
This brings up an issue that has a bearing on irreducible complexity. To illustrate my point I'll use some homemade phrases. IC systems can be thought of as layered. Some are more basic to the overall function of a cell than others. These functions in general could be thought of as having been conserved at the outset. For example, a protein found in a cellular membrane could have a vital function. But its synthesis is dependent on other proteins that are more basic to overall cellular function in that they also are involved in the synthesis of other proteins unrelated to the cellular membrane protein. As a general rule the more basic the protein function, the more difficult it is to detail a plausible pathway to its origin IMO. If this is so then it is the most basic of proteins in IC systems that should be the object of inferences for ID.
Comment by Bradford — March 2, 2007 @ 4:51 am
March 3rd, 2007 at 2:51 pm
Bradford, you wrote,
Your answer has nothing to do with my question, so perhaps my question was unclear–a lot of practicing biologists confuse specificity with selectivity.
When I used the term "selective" in my question, I was not referring to selection in evolution–I was using it as a biochemical term. Selectivity (for protein-protein interactions/enzymes) is well-defined as binding/using a range of partners/substrates, some better than others, and can be measured. Since Guts doesn't seem to be interested in this question, would you mind having a go at making a prediction, assuming I've clarified the question sufficiently?
You also wrote,
Obviously, the analysis would take longer to complete. But wouldn't the amount of time required to develop protein-protein binding in this way be highly relevant to deriving a new function from any existing system that meets the ever-shifting definition of IC?
But isn't that related to my question (hopefully now clarified) about specific vs. selective interactions? Do the proteins you consider "most basic of proteins" exhibit specific or merely selective interactions with other proteins and substrates?
Comment by genomic — March 3, 2007 @ 2:51 pm
March 3rd, 2007 at 5:35 pm
They are specific, interacting with just one or only a few substrates and they catalyze a specific type of reaction.
Comment by Bradford — March 3, 2007 @ 5:35 pm
March 4th, 2007 at 2:34 am
Bradford, if they interact with only a few substrates, they are selective, not specific. Would you mind identifying some of the specific ones? I'd be interested in the selective ones, too, but not as much as the ones you deem to be specific.
Comment by genomic — March 4, 2007 @ 2:34 am
March 4th, 2007 at 3:17 am
genomic, it appears that you could identify your own protein example to illustrate whatever point you intend to make. I don't know why you want me to designate a protein but I'll play along. Ubiquitin. What do you wish to do with ubiquitin?
Comment by Bradford — March 4, 2007 @ 3:17 am
March 4th, 2007 at 1:28 pm
My point relates to making false assumptions in lieu of making and testing predictions.
So you're offering ubiquitin as an example of a specific enzyme? Are you claiming that ubiquitination is specific for lysine residues, or are you predicting that as a hypothesis that you are interested in testing?
Comment by genomic — March 4, 2007 @ 1:28 pm
March 4th, 2007 at 2:54 pm
We already know ubiquitin forms covalent bonds with other proteins at ubiquitin's C-terminal end; the location of a glycine residue. Lysine side chains of other proteins are part of the bonds. This does not need testing. What assumptions are you making about ubiquitin that is relevant to whatever it is you believe?
Comment by Bradford — March 4, 2007 @ 2:54 pm
March 4th, 2007 at 6:20 pm
genomic writes:
No. What I said was "protein interactions aren't easily generated", I then linked to a post that links to a paper that shows how a single change is not sufficient to generate Na+ binding and activation (a single change is sufficient to abrogate it). This suggests that protein-protein interactions aren't necessarily easily generated either.
genomic:
I don't see how that follows.
Comment by Guts — March 4, 2007 @ 6:20 pm