Uncommon Descent Serving The Intelligent Design Community

Many genes relatively new, scientists find

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Science writer Carl Zimmer in the New York Times on recent discoveries in the ongoing evolution of genes:

New genes were long thought to derive from duplications or mistakes in older genes. But small mutations can also form new genes from scratch.

For some scientists, like Dr. Tautz, the data pointed to an inescapable conclusion: Orphan genes had not been passed down through the generations for billions of years. They had come into existence much later.

“It’s almost like Sherlock Holmes,” said Dr. Tautz, citing the detective’s famous dictum: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”

Dr. Begun and his colleagues renamed orphan genes “de novo genes,” from the Latin for new. He found that many of his fellow scientists weren’t ready to accept this idea.

Can’t think why not, can you? 😉

While many de novo genes ultimately vanish, some cling to existence and take on essential jobs. Dr. Tautz said the rise of these genes might be as important a factor in evolution as gene duplication.

Now how will this affect attempts to construct evolutionary histories via genome mapping?

More Zimmer on the genome:

One gets the impression that the guy who thought our genomes were in some sense “us” spoke too quickly.

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Comments
@UB In that case I can't see which part of what I'd written made you so aghast. Querius's question was about determining common descent in linguistics (i.e., about common ancestors), so I simply replied to that. I did not declare any lack of interest in "physical processes". So much for reading comprehension.Piotr
May 3, 2014
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Piotr You should practice a little more disciplined reading comprehension. There is nothing I wrote that had anything to do with a single common linguistic ancestor. My comment was about the physical process. I think I made that most abundantly clear.Upright BiPed
May 3, 2014
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@Upright Biped We all have the same language faculty (biologically grounded ability to learn and use a language). It doesn't logically follow that all languages spoken today had a single common ancestor or that there was ever a time when the whole human population spoke one language. The former is barely possible (but far beyond our current ability to prove such a thing); the latter is highly unlikely. "Being related" has a concrete definition in linguistics: it means being demonstrably derived from a common ancestor, not just being a similar type of code. Perhaps you would not be so aghast if you'd had a little training in historical linguistics.Piotr
May 3, 2014
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We don’t know at present if all extant languages are ultimately related.
Each and every one of them is indisputably related by the singular physical conditions by which they operate in the material world. These are precisely the same physical conditions as those found in the translation of the genetic code. I'm just aghast that a person with a background in language would not see the interest in this demonstrable fact. The unique process by which physical effects are produced from language and mathematics are found nowhere else in the cosmos except in the translation of the genetic code. A physical capacity that would not appear in the historical record (from our perspective) until the rise of humanity, was not only clearly present at the origin of life, but is the manifest physical reason life on this planet exists.Upright BiPed
May 3, 2014
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Mapou: I agree. Of course designers are strongly influenced by previous designs. There are logic connections, in biological design, which can be studied and analyzed, once the design paradigm is accepted. And, as already said, languages evolve with the constant influence of conscious beings.gpuccio
May 3, 2014
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Please, don’t expect me to take him seriously.
You have just pigeon holed yourself as not a serious commenter.jerry
May 3, 2014
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What evidence supports your assertion that there’s close analogues between biological evolution and the observed changes in languages?
Why would this be a plus for Darwinian evolution and not also for Design evolution? I think that hierarchical evolution makes perfect sense within the Intelligent design paradigm. Designs do evolve over time simply because designers come up with new designs that are strongly influenced by previous designs.Mapou
May 3, 2014
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Let me begin with this one.
How do linguists judge common descent between languages? Is there a tree of life in language and did they all start from a single language as current OOL theories suggest in the realm of biology?
There is good evidence of relationship for some groups of languages. For example, English is related not only to German, Dutch and Swedish (which shared a common ancestor about 2000 years ago), but also -- much more distantly -- to Greek, Latin, Irish, Russian, Lithuanian, Hindi, Farsi, Armenian, Albanian, and many others within the so-called Indo-European family. There are many established language families: some with hundreds of members, some smaller, some consisting of a single language (for example, Basque). To judge common descent we use the so-called comparative method, which is not very different from what biologists do. In a nutshell, we look for demonstrable homologies. We don't know at present if all extant languages are ultimately related. It's a possibility, but we simply haven't got enough information to prove long-range relationships. The known families consist of smaller units (also united by common ancestry), like Germanic, Slavic, Celtic, etc. There's a lot of horizontal transfer (borrowing) between languages, which often has the effect of blurring genetic relationships in the long run. It's a vast subject and I wouldn't like to developp it here. Anyone interested in historical and evolutionary linguistics is welcome to my blog, where I discuss such things. I haven't posted there for a few months, but intend to continue soon.Piotr
May 3, 2014
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The worst that can happen is that we go on disagreeing, without even being able to understand why.
I disagree. ;-) The worst thing is ad hominem attacks. I would ask Piotr what actually drives change in languages. Chance and necessity? Natural selection? A desire to alienate from another population? Changes in thought processes and cultural values? How would one be able to tell the difference between a synthesized language and a "natural" language? How do linguists judge common descent between languages? Is there a tree of life in language and did they all start from a single language as current OOL theories suggest in the realm of biology? Why does Latin seem more complicated than current Romance languages? What's different between now than then? What evidence supports your assertion that there's close analogues between biological evolution and the observed changes in languages? -Querius (a blend of query and curious)Querius
May 3, 2014
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@Jerry Sorry if you found my judgement of Wilcox's talk too summary, but it's really a lot of nonsense despite the "hundreds of references". Please show me one research paper which claims that human regulatory networks are "incredibly more complex" than those of a chimpanzee (or any other mammal, for that matter). Are there any such reports among the numerous articles cited by Wilcox? I don't think so. Nor do Wilcox's theological preamble and the discussion of questions like the original sin further in the same presentation inspire much confidence in the quality of his biological argument. He also swallowed the ENCODE hype hook, line and sinker. Please, don't expect me to take him seriously.Piotr
May 3, 2014
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Joe, jerry: Let us leave Piotr free to express his ideas. We are here to debate with those who think differently, after all. Piotr has been a good listener, until now, and at least the discussion has become specific and technical, which is always a good thing. Moreover, being a linguist, he could be more open-minded than a biologist. Let's see. The worst that can happen is that we go on disagreeing, without even being able to understand why.gpuccio
May 3, 2014
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As if I needed more evidence that Piotr is on an agenda.
Most people who come here know only what the majority are saying and assume we are religious crackpots. After all there are some here who would qualify as such. i am sure Piotr is the same. He is a linguist and languages have definitely evolved over thousands of years. Also most people looks at dogs and other such animals and see how they come in very different physical shapes and assume that over million of years that natural processes could do the same. But he does not seem to understand that the information changes necessary for evolution are not as simple as that for languages or dog breeding. He seem to assume that small random changes will build the necessary proteins when we know it cannot. Most of the naturalists who come here assume that. Allen Fox till he disappeared here would constantly say that Axe and Durston were wrong. Fox would try to have a debate with Durston and tell him why his ideas and research were bogus.jerry
May 3, 2014
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OK I went to Dan Graur's blog and found many bald declarations but nothing wrt an interesting discussion. As if I needed more evidence that Piotr is on an agenda.Joe
May 3, 2014
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gpuccio- If Piotr knew anything about biology he wouldn't be making the claims that he is making. Right now all we have is his say-so, which is meaningless regardless of what he does for a living- so you are correct and I was wrong.Joe
May 3, 2014
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Piotr: For your convenience, I will try to briefly sum up the concept of function in defining dFSCI: a) We have an object from which it is possible to objectively read some digital sequence according to some possible rule. Any rule can be applied, provided it is objectively stated, so that any observer can derive the same sequence with that rule. b) An observer can propose any possible function for the object with its sequence. What is a function? Simply a way we can use the object and its sequence to obtain some well defined result. Again, the function must be objectively defined, and the observer must give an objective way of measuring it, and if necessary a threshold to categorize it in binary form. c) For each function defined in that way, we can compute a functional complexity. If the function is referred to the digital sequence, the computation is easier (that's why I use the dFSCI concept). It is essentially -log in base two of the ratio bewteen the number of functional sequences of that length and the number of possible sequences of that length (the target space/search space ratio). This is just the essential. Those concepts can be applied to any digital sequence: language, software, protein coding genes.gpuccio
May 3, 2014
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Piotr: Well: "Because genomes are products of evolution rather than “intelligent design,” all genomes contain functional and nonfunctional parts. " is not exactly a promising way to begin, at least for me. :)gpuccio
May 3, 2014
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Piotr: "One of the reasons why I’m so interested in the concept is that it has very close analogues in theories of language variation and change." Obviously! That's the first thing I thought when you said that you are a linguist. But let's remember that language is born and changes in part because of conscious experiences. :)gpuccio
May 3, 2014
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Piotr: "Do you mean that evolution is about to end soon, as new proteins get shorter and shorter? ;)" Maybe you are not serious here, but I really think that evolution will go on, but it will be mainly non protein evolution (non coding genes, regulatory elements, procedures).gpuccio
May 3, 2014
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By the way, there's an interesting discussion of biological "function" on Dan Graur's blog. Very timely. One of the reasons why I'm so interested in the concept is that it has very close analogues in theories of language variation and change.Piotr
May 3, 2014
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Piotr:
So you are prepared to accept that at least minor functional innovations can occur “by themselves” and do not require the supernatural designer’s personal intervention. Is that right?
Sure. My position is clear. We can infer design through functional complexity, and in no other way. The threshold is debatable. For the moment, I will stick to 150 bits (35 AAs). I will not make design inferences for lower functional complexities. However, my reasonable conviction is that Axe is right, and that the true edge of biological random evolution is about 5 AAs. Of course, the more the data, the more we can focus those issues. And please, take all the time you need.gpuccio
May 3, 2014
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Joe: I say this with the greatest respect for you: I agree with you in many things, but why criticize Piotr because he is a linguist? Let's judge what he says. Authority has no special role here, IMO, while good arguments are good, whoever expresses them.gpuccio
May 3, 2014
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And I have offered my reasonable explanation: of the length of taxon restricted genes constantly increases with their age, it is probably because the functional requirements for new proteins are different as evolution goes on.
Do you mean that evolution is about to end soon, as new proteins get shorter and shorter? ;)
That’s exactly why I believe in common descent.
Good! There is enough common ground to make discussion possible.
Of course, there are many cases of tweaking of the function in a family, sometimes with the appearance of a new function, but related to the old structure and function. Nylonase is a good example. Many of those cases are not very complex, implying only a few aminoacids’variation at the active site.
So you are prepared to accept that at least minor functional innovations can occur "by themselves" and do not require the supernatural designer's personal intervention. Is that right? [I'm sorry if I don't reply at length yet. I'm a little busy today and can't spend the day glued to the keyboard, but I'll be back soon.]Piotr
May 3, 2014
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Piotr: Just a comment on this statement of yours to Mung:
I would say that the accidental origin “from scratch” of a gene encoding for a complex functional protein is practically impossible, while the accidental emergence of functionality in a small protein with a random amino acid sequence is possible despite its small probability (see Szostak’s experiments with ATP-binding short proteins randomly generated in vitro).
Without entering in detail here (I have already said too much) I must at least mention that I have criticized extensively that specific paper here, in the past. Szostak has clearly used intelligent selection in the procedure, and his conclusions are not applicable at all to random sequences.gpuccio
May 3, 2014
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Piotr: Some other aspects I would like to clarify. I am more than ready to account for the fact that "the mean length of taxon-restricted proteins (which might plausibly have a de novo origin near the root of the taxon) increases with their age". Facts must always be taken into consideration. And I have offered my reasonable explanation: of the length of taxon restricted genes constantly increases with their age, it is probably because the functional requirements for new proteins are different as evolution goes on. At OOL and in the first stages, a lot of new superfamilies had to be designed in a relatively short time, and they had to cover a lot of basic biochemical "miracles", without which life could not exists. As time goes by, and design focuses more on the expression of new functions, built on the basic functions that already exist, the type of protein required slowly changes. In the last phases, new proteins are mainly requested for specific, high level regulations, while most of the functional novelty comes from modifications, still only partially understood, in non coding DNA or other regulatory structures (epigenetic). This is, IMO, a very reasonable scenario. It explains not only the lower length of new taxon restricted genes, but also the slowing rate of appearance of new superfamilies, and the highest modular multidomain structure of ancient proteins. I want to specify, too, that the variations we see in proteins through time, and which are so emphasized by neo darwinism, are essentially of one kind: Once a new protein superfamily or family, with a defined new structure and function, appears for the first time, it is already unrelated at sequence level with what already exists (that's implicit in the definition of superfamily: no detectable homologies with the others). Then, as time goes by, and new species appear, what happnes is: the protein essentially maintains its strucure and function (with possible tweakings), but the sequence diverges. The typical case is similar to proteins like Glutamate–tRNA ligase and Alanine-tRNA ligase, which show still a strong homology between the bacterial form and the human form, usually 30-40% of identities and 50-60% of similarities. Anyway, the sequence is different for a good part, about half of it, but the function is exactly the same: they couple the right aminoacid to the right tRNA. If they did not work correctly in all species, no translation could take place, and life could not exists. Just to give an idea, between human and mouse those two proteins have 85% and 96% identity. And still they do the same thing. That's exactly why I believe in common descent. What is the reason for that? The best explanation is: The proteins, after they appear for the first time with their functionality, "traverse" their functional space in the course of evolution, because of neutral variation which modifies the function, but do not abandon it, because of negative selection which eliminates most non functional forms. That is what is usually called "the big bang theory of protein evolution". Big bang: a new protein appears the first time, with a functional sequence, and then neutral evolution expands the space of sequence, without modifying structure and function. That's what we see in the whole proteome: isolated superfamilies, and then great divergence in the context of the same superfamily or family. Of course, there are many cases of tweaking of the function in a family, sometimes with the appearance of a new function, but related to the old structure and function. Nylonase is a good example. Many of those cases are not very complex, implying only a few aminoacids'variation at the active site. And of course, there are proteins which are much more conserved between their first appearance and humans, like ATP synthase subunit beta, or RAG1, with their 72% and 59% identities, showing greater than usual functional constraint of the sequence, and resistance to neutral variation.gpuccio
May 3, 2014
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Piotr's problems: If you have a small and functional protein, that means it has a substrate, the portion of the protein that catalyzes a reaction. If you add on to that protein you are going to bury that substrate which means it may not be accessible depending on whether any properly charged channels were left open to said substrate. Yes the channels have to be properly charged or else the materials required will not make it to the substrate. Then you need properly charged channels for exiting the protein once the reaction is finished. Doug Axe goes over this in his essay in "The Nature of Nature" see catalase (for example)Joe
May 3, 2014
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Piotr:
I’ll soon return to the question whether proteins may get longer and more complex in the course of time without intelligent guidance
Hopefully you have some actual evidence. The say-so of a linguist is meaningless.Joe
May 3, 2014
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Piotr:
I’m taking part in this discussion at my peril, out of my personal curiosity, and represent only myself. Any errors or knowledge gaps are entirely my own.
That's absolutely true of me too (by the way, I am a medical doctor). That's how I like it. And I am enjoying the discussion too! As I said in the beginning, you are a very good adversary.gpuccio
May 3, 2014
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@gpuccio:
You suggest that it is evidence that they are young and therefore scarcely functional, and that function evolves with protein length in time. I say that there is no evidence of this strange theory. Protein families have long or short sequences according to different functional requirement, not according to how old they are.
That's why I asked you if you accepted evolution (even assuming that it was intelligently guided) and the phylogenetic time depths established by mainstream science. If so, you should somehow account for the fact that the mean length of taxon-restricted proteins (which might plausibly have a de novo origin near the root of the taxon) increases with their age. I'll soon return to the question whether proteins may get longer and more complex in the course of time without intelligent guidance, responding both to you and Mung. I have to say I'm enjoying this discussion. It's quite stimulating. A small DISCLAIMER is perhaps in order: -- I'm a linguist, not a biologist, so don't expect me to be a spokesman for professionally practised evolutionary biology. I'm taking part in this discussion at my peril, out of my personal curiosity, and represent only myself. Any errors or knowledge gaps are entirely my own.Piotr
May 3, 2014
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Piotr: Another important aspect. Please, look at the following recent paper: "Emergence of novel domains in proteins" http://www.biomedcentral.com/content/pdf/1471-2148-13-47.pdf The point is: new domains have the same length as old domains (about 150 AAs is the mean, and indeed mammalian domains are a little beat longer than old ones), while old proteins are often longer than younger ones, and the simple reason is that they have higher domain numbers (see Table 1 and Table 3).gpuccio
May 3, 2014
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Piotr: To sum up: a) I believe that the lower length of new genes in more recent species can be interpreted according to different functional requirements, essentially regulatory. b) You suggest that it is evidence that they are young and therefore scarcely functional, and that function evolves with protein length in time. I say that there is no evidence of this strange theory. Protein families have long or short sequences according to different functional requirement, not according to how old they are. IOWs, length variation is maximal between families, and is minimal inside one family. To show my point, I have collected some data about 6 different important and old proteins, proteins which appeared "at the beginning", and which are still there, in humans. I have taken 3 aminoacyl tRNA synthetases and 3 glycolisis enzymes. Here are the data: The proteins: 1) Glutamate--tRNA ligase 2) Valine--tRNA ligase 3) Alanine--tRNA ligase 4) Pyruvate kinase 5) Triose phosphate isomerase 6) Phosphoglycerate mutase The data: E. coli Id C. El Id Human Elong. 1) 471 31% 481 38% 523 11,04% 2) 951 40% 1050 54% 1264 32,91% 3) 876 39% 968 58% 968 10,50% 4) 470 46% 558 58% 574 22,13% 5) 254 48% 247 62% 286 12,60% 6) 413 50% 434 75% 434 5,08% There is the length in E. coli, in C. elegans and in humans, and the % identity with the human proteins. Finally, there is the percent elongation of each protein from coli to human, which, as you can see, is present but small (from 5% to 32.9%). Instead, the variation in length between different proteins in coli is much large, from 254 to 951, a 274% difference. Which is exactly my point. I believe that the small increase in length inside a family can be easily explained in terms of adaptation to different, and more complex, cellular contexts, while there is no reason to believe that it is related to an increase in the basic function, which, as far as we know, is efficiently performed by all these proteins, each one in its cellular context.gpuccio
May 3, 2014
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