A second highly selected gene, LYST, is associated with pigmentation, and changes in it are probably responsible for the blanching of the ancestors’ brown fur. Computer analysis for the multiple mutations of the gene showed that they too were almost certainly damaging to its function.
In fact, of all the mutations in the seventeen genes that were most highly selected, about half were predicted to damage the function of the respective coded proteins. Furthermore, since most altered genes bore several mutations, only three to six (depending on the method of estimation) out of seventeen genes were free of degrading changes [fn 2]. Put differently, 65 to 83 percent of helpful, positively selected genes are estimated to have suffered at least one damaging mutation.
- Darwin Devolves p. 21
fn 2 is Table S7 of Liu et al.
Can we work through this one item at a time to see what people agree with or disagree with?
Here sciencedaily cites a study on LDL-C levels, but I don’t have access to it.
You good you! 😉
That would be covered in one of my upcoming OPs…
Here’s a PDF
That doesn’t support your contention at all. I think you forget what you wrote:
You’re supposed to find papers that show that animals with a high rate of blood cholesterol clearance are worse off, aka that their “efficient clearing” of blood cholesterol is “detrimental to animals with a diet which is less fatty than that of polar bears”.
It should also be noted that the question of the potential health issues with high LDL (and low HDL) cholesterol is very controversial, and that there is lots of research that contradicts the one you found, not that this is really essential to the point I asked you to support. Which you have still not done.
From here
How do you think this cholesterol gets to where it’s needed if not by transportation through the blood system? So it is as I have already said, the correct balance of cholesterol levels in the blood needs to be maintained. Why would an animal go to the trouble of producing cholesterol in the liver only to efficiently clear it from the blood before it can be used?
Not if it stays in the blood obviously. It gets into the blood, is then transported by circulation, and then needs to be put back where it is actually used instead of staying in the blood stream.
Why do you think it isn’t being used if it is effectively cleared from the blood? You seem to think clearing it from the bloodstream makes it go out of existence, instead of merely being effectively absorbed into the tissues where it is needed.
Ironically it is you who have a too simplistic notion of what these words mean.
Uhh please cite the literature that shows this. Not buying it.
Where does he say this? This is your gloss on what Behe says and it is false.
swamidass,
He spends time in his book talking about neutral theory and its potential contribution. What are your specific comments on his discussion of neutral theory?
ROFL.
So Mung let me please have some clarification here. Is it your contention that Behe thinks genetic mutations mutation, drift, selection, endosymbiosis, and neutral theory, is sufficient to account for the diversity and complexity of life?
Michael Behe:
I think people have been interpreting Behe’s comment in the most unfavorable light possible. First, it’s unclear what he means by “relevant information.” Second, it’s unclear whether his reference to “the table” is to the list of damaging or possibly damaging mutations he provides on the website or to table S7 from teh original document.
What the list on the website shows is a list of genes all with damaging or possibly damaging mutations. I do not believe that Behe meant to convey that all mutations in all those genes were damaging.
T_aquaticus,
Did you read the book?
But then Behe showing that list does not substantiate his claim that most adaptive molecular evolution, aka most adaptive mutations, are of the “breaking/blunting” type.
For Behe’s argument to make sense he has to show the relative frequencies of damaging adaptive, versus non-damaging but still adaptive mutations. To carry his thesis, he needs to show that there are more damaging than non-damaging adaptive mutations.
Otherwise the “first rule of adaptive molecular evolution” would be to “mostly non-damage and instead simply modify genes”. Right? The kind of change that happens most frequently is the kind of change we would describe as the “first rule” of adaptive evolution. If the kind of change that happens most frequently isn’t actually damaging, but “benign”, then his rule needs to be re-worded, and his book should be called “Darwin modifies”.
Now that’s a convincing retort! You make Behe come off as anti-evolution. He is not.
“…the conclusion that the molecular and functional complexity of life could not have evolved.”
Demonstrably false. In fact, he admits polar bears could have evolved.
Behe comments:
So true.
By the way, Rumraket, I appreciate your contributions in this thread. Are the insults really necessary?
I don’t think you should be using his 2010 paper as an interpretive guide to the book. The book is written for a popular audience who will not have read his prior paper and may not have even read any of his prior books. The book should stand or fall on its own based on the content in the book. What do you think?
I don’t think that was the point of showing that list.
They should have had you write the Science review. 🙂
Still catching up with the original Polar Bear article to see what is meant by “benign.” I think the important element is whether or not they are considered to be adaptive. Is that the way you take it?
This makes no sense. And you, Joshua, are the one who defines Darwinism as “positive selection dominated change.” So you hammer him for doing the exact same thing you do. Are you just oblivious to that fact?
ROFL, Mung. Nice try, but you missed a word. Perhaps you are unclear on what Behe means by “the relevant information”. In English, that phrase, with the definite article, is used to refer to the totality of the relevant information.
The table that he went to the effort of constructing, carefully cherry-picking the data that he wants to show his gullible audience and eliminating every single “benign” mutation, that table is the referent, and the condescension of “Those who can understand the table” precedes a second false claim.
That’s a weird turn of phrase, Mung. Behe shows a list of mutations, all of the “potentially” and “probably damaging” mutations, and none of the “benign” ones, in the genes under study. I agree that Behe did not want to convey that all mutations in all those genes were damaging. Behe’s goal was to obscure the issue as much as possible, preferably without falsehood.
That’s pretty much the entirety of his work product. Evey now and again (e.g. LYST) he slips up and his circumlocutions are actually false, rather than merely misleading.
P.S. You ran away from our conversation on the Three Musketeers thread:
Do you really mean mutations, rather than genes? If so, how does he spot them?
You can’t possibly believe that.
There’s a difference between polar bears evolving from brown bears, and the all complexity and functionality of life evolving. Behe seems to think evolution can’t produce an increase in complexity, only a reduction.
I have not made any bizarre absolutes about Behe’s claims. It’s totally straightforward. Behe is attempting to show that the functionality and complexity of all the diversity of life could not have evolved, because the rate of “degeneration” would always be higher than the rate of “construction”, so that there would, on average, always be a net loss of “functional complexity”, if if weren’t for the actions of the intelligent designer. So the designer creates the complexity, which then slowly degrades. That’s his “big picture” view of evolution. Please Mung, don’t try to pretend not to get that this is the message of his book.
Well if you’re prepared to even deny the obvious take-home and intended message of a book titled “Darwin devolves”, then I’m not going to respect your opinion.
If you extend to me the courtesy of acknowledging the central message that Behe intends the reader to take from his book, we can proceed with some regained mutual respect. Can we at least agree on what Behe’s central message of the book is? If you disagree with what I wrote above, can I then get you to state as unambigously as you can what you think the central message of the book is?
I think Behe is an ID proponent, and I think Behe is an ID proponent in part because he believes evolution is insufficient to account for the complexity and functionality of the diversity of life, and that with this book he is intending the reader to come away with a similar viewpoint, that evolutoin mostly degrades and breaks stuff, rarely creates anything, and when it does it is too little to stave off the overall degenerative process.
I read what is publicly available on Amazon, and on the later pages of the book one can see there, Behe is using terms he first invented in his 2010 paper. That leads me to suspect that Behe does in fact, somewhere, in his new book, try to analyze things in terms of concepts he has defined in that paper.
DNA_Jock,
blockquote>
Have you read the book?
On the meaning of benign:
As I read this, all three are “damaging” with varying degrees of probability. Is that how others read this?
See my post above.
What’s the book about? From what I’m reading now it’s about the power of natural selection to make do. No Intelligent Designer required.
Behe is attempting to show that the functionality and complexity of all the diversity of life could not have evolved without intelligent design. It could have evolved with intelligent design.
Something else I’d like to ask people about:
Are there two different results, one for polar bears and one for humans? And S7 is for the former not the latter?
Does Behe actually argue how ID solves the purported problems he claims he’s found in evolutionary processes?
Part IV: Solution
How long is part IV? Can you please summarize it in a few sentences?
No, there are not. PolyPhen-2 predicts the likely effect of mutations in human genes. In fact, HumDiv assumes that observed inter-mammalian variation is not damaging. Its application to bears is outside of its intended scope.
Haven’t you wondered why we keep putting “benign” and “damaging” in quotes, FFS?
Sure, it could have evolved with Intelligent Design (read: divine intervention). But which ‘intelligent design’ could have evolved it ‘externally’? Your referent, like Behe’s no doubt, is intentionally empty, as if ‘it doesn’t matter’ when it actually does matter. This is an obvious flaw in IDism’s logic.
No. Are you going to answer the second question? Is S7 for polar bears or humans?
Ask first, is it useful in the niche!
Right, so my description was correct. Life, according to Behe, could not have evolved to it’s current diversity and complexity because the mechanisms of evolution are primarily “degenerative” without the aid of some sort of intelligent design.
So when I said:
Rumraket: The problem is that Behe takes his “first rule of adaptive evolution” to the conclusion that the molecular and functional complexity of life could not have evolved.
… And you responeded:
Mung: Where does he say this? This is your gloss on what Behe says and it is false.
It was actually true what I said. Now we can proceed to analyze whether the claim is correct, that life could not have evolved without intelligent design, because of Behe’s purported “first rule of adaptive evolution”.
I did answer. S7 is the application, to mutations observed in polar bears, of a predictive algorithm for human genes.
In order to gauge the better explanation, what is the proposed manner in which the intelligence reverses the degenerative effects of Evolution and implements the the diversity?
Humans. From suppplementary information:
So according to the software, roughly fifty percent of mutations were predicted to be more likely than not of being damaging. That is at best a whitewash. Another problem here is that the software can only predict “damaging” or “benign” with different probabilities, and that in fact some mutations might not even be damaging at all, and are only scored as such because the PolyPhen-2 software is trained on human disease data.
From this publication on how the software works: A method and server for predicting damaging missense mutations
“For a mutation, PolyPhen-2 calculates Naïve Bayes posterior probability that this mutation is damaging and reports estimates of false positive (the chance that the mutation is classified as damaging when it is in fact non-damaging) and true positive (the chance that the mutation is classified as damaging when it is indeed damaging) rates. A mutation is also appraised qualitatively, as benign, possibly damaging, or probably damaging (Supplementary Methods).”
We can see in supplementary methods the following:
” For a mutant allele, Naïve Bayes approach produces the likelihood that this allele affects protein function, phenotype, and fitness, or, in other words, is damaging, as opposed to benign.”
So in fact it can only score mutations as damagning-or-not, which is actually based on the assumption that a function-altering mutations will be selectively deleterious (or functionally disturbing, phenotypically altering in a negative way) because a similar mutation in human has somewhere been estimated to cause a disease.
But these very same mutations were positively selected in polar bear. What this means is that the software actually doesn’t have a clue what these mutations do in polar bear, and their effects on humans is only a weak indication at best. Meaning it is likely that the false positive rate is higher than “normal” for this software when considering the effects of these mutations in polar bear.
To me, this complaint of ID as not being science is a bit like claiming that work with gravity is not science, because we don’t know what gravity is. As if it doesn’t matter what gravity is. Same thing with quantum entanglement. If we don’t know what causes this entanglement, how is that science. Its intentionally empty. This is quantum mechanics flaw in logic. We don’t know the mechanics so how can we call it mechanics?
That’s why you are not a scientist.
Ah, the problem is your usage of the “we” there. You don’t know =! everybody does not know.
Mung,
Crikey, thought I was reading a criticism of the ID types hereabouts at first.
One general comment I would make is that it is false reasoning to pin too much of historic evolution on principles applying to recent species. Even if there weren’t much scope for ‘constructive’ novelty these days, and evolution was restricted to ‘destructive’ tinkering, it does not mean that this situation pertained throughout the history of a given lineage. Similarly, one can’t assume that the presence of modern organisms on adaptive peaks, where most amendments are ‘downhill’ or deleterious, precludes them from having got there in the first place.
Great!
Your link seems to be broken 🙁
Fixed.
Yes, that was a bit of confused writing on my part. But on the plus side I’m learning a fair bit about cholesterol, where it originates, how it is distributed, all the bodily processes it is involved in, that sort of thing. So I’m learning a lot from my mistakes 🙂
And there is wisdom in these processes. In order to stay healthy we need to maintain a suitable balance within the ideal range of our body mass index (BMI). For a polar bear to stay healthy it needs to maintain a much higher BMI.
Natural selection ensures that they maintain an ideal BMI. It fine tunes the organism to its environment. We humans have risen above the stage where we have to rely on natural selection. We have been given the responsibility of looking after ourselves and that is why those who have the means very often become obese. And those who don’t have the means,well, as long as we that have, have, and who cares about the rest? That is the price we pay for being given this freedom.
Yes more confusion on my part.
But to get back to the main point on Behe’s focus on damaging mutations, here’s how I see it:
Say a plastic surgeon made several modifications to the face of a patient. All of the modifications were purely cosmetic except one. Only one the modification had any effect on function. Say the surgeon cut through a nerve which prevented the patient from moving the left side of their mouth.
Would we say that the overall effect on the patient (gene) was that they had suffered damage or that there was no effect on them?
Or to use another analogy, if a body has several benign tumours and one cancerous tumour does the ration of one type to the other really matter?
It doesn’t matter the ratio of benign to damaging mutations there are, as a whole the gene can be said to have been damaged if there is just one damaging modification present.
CharlieM,
Don’t know if anyone has mentioned exaptation to you. This talk of “damaging” mutations is based on an analysis intended to spot possibly pre-cancerous mutations. So a change resulting a loss of function is not necessarily damaging to the organism if there is the possibility of a new use for a protein (or system) that no longer functions in its original role. Melanin loss in body hair causing bears to be less visible to potential prey is such an exaptation, an advantage when bears encountered the new niche of the arctic.
ETA exaptation
Let me stir the pot a little.
Complete loss of LYST gene function in humans results in Chediak-Higashi syndrome, a heritable disease associated with decreased pigmentation of hair (hey surprise!) but also partial albinism, immunodeficiency, coagulation defects, varying neurologic problems and peculiar malignant lymphoma. Death often occurs before the age of 7 years. Assuming LYST serves a similar function in polar bears as in humans, it is apparent that it has not completely lost all of its former gene functions.
The reason for this pleiotropic behaviour is that LYST is not only expressed in melanocytes of hair follicles, but ubiquitously expressed to regulate vesicular transport. Therefore, it is also required for e.g. the proper function of cytotoxic lymphocytes, in particular natural killer cells. Now, this is all speculation of course, but it seems to me that since polar bears are not suffering en masse from Chediak-Higashi syndrome that LYST must still capable of performing its ancestral molecular function, despite it having accumulated several “harmful” mutations. It thus appears that LYST function was selectively decreased in follicular melanocytes, because of its adaptive value. How smart of blind non-intelligent natural selection.
Corneel,
Indeed. Polar bear skin is heavily pigmented with melanins, (black in other words).
Thanks.