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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
My explanation is simple: I reject your assertion that protein length can’t evolve.
And when you have some evidence to support your "explanation", someone will listen.Joe
May 2, 2014
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Piotr:
I do not claim that all proteins evolve by consistently increasing their length and complexity — only that they begin their evolutionary career as relatively short and unsophisticated structures.
That's right. And we're not saying you contradict yourself, for you are obviously arguing that not all proteins are long and sophisticated. Especially not the young ones. But it's a reasonable inference on our part, is it not, that you do believe that older proteins started out just like younger ones, as relatively short and unsophisticated? Relative to what? The older and relatively longer and more sophisticated proteins did not just pop forth that way de novo, did they? And that's the question gpuccio is asking you. What's your evidence for the gradual increase in length over time and increased specificity over time and heightened complexity over time of the older proteins? How are you not arguing in a circle? See my post @ 71.Mung
May 2, 2014
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Jerry:
Control mechanisms in the human genome are apparently incredibly more complex than its nearest so called cousin, the chimp.
Have you got a reference for that? It's widely believed that the differences between humans and chimps are mostly due to differences in gene regulation, but it doesn't follow that the regulatory networks of the human genome are "incredibly more complex". They are just different for some key genes.Piotr
May 2, 2014
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Joe:
Nothing and obviously it happened at the OoL- the intervention event. However now there isn’t any intervention now. Organisms have to rely on their built-in responses to environmental cues- most of which occur within the immune system- something else that unguided evolution cannot explain.
A fine statement of young earth creationism. God started it all off then it was hands off, everything else mechanistic. Evolution. Can we call this intelligent PRE-DESIGN so as to distinguish it from intelligent design? Does part of that pre-design preclude species from eventually evolving into new "kinds"?Mung
May 2, 2014
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Now, if this important protein appeared in jawed fish, and if it retains practically the same length and sequence in humans, it is obvious that it had more or less the same length and sequence when it appeared in the first jawed fish. IOWs, when it was a de novo gene. How do you explain that?
How do you know what it looked like when it started evolving de novo? The protein was apparently complex and well conserved already in the last common ancestor of humans and zebra fish. But was the gene encoding for it a true de novo one at the time? It seems to have homologues among the Transib transposons, and its core sequence has been found in other deuterostomes (amphioxi and echinoderms). See https://en.wikipedia.org/wiki/Recombination-activating_gene#EvolutionPiotr
May 2, 2014
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In Durston’s paper, the minimum functional complexity found is 46 bits, for Ankyrin, which is 33 AAs long. All proteins longer than 65 AAs have more than 150 bits of functional information (except one which is 123 bits). Unless de novo genes are completely different from all other functional proteins we know of, their functional complexity cannot be explained by random variation.
I suppose you mean Durston's "fits", units related to, but not identical with ordinary "bits". Is there a magic threshold above which complexity is not evolvable? If so, what is it and how do you know?
Proteins are longer when they are older. But that’s not because they start short and gradually become longer. Older proteins start longer, and more recent proteins start shorter. And remain shorter.
OK, I'll repeat ad nauseam if necessary: why should it be the case?
As I have shown you with the example of ATP synthase, proteins do not grow in length and complexity with time. I could give many other examples.
If they are very important and highly conserved, stabilising selection conserves their size as well. It doesn't mean that the ATP gene family sprang into existence ready-made. I do not claim that all proteins evolve by consistently increasing their length and complexity -- only that they begin their evolutionary career as relatively short and unsophisticated structures.
Your theory, that proteins start short and scarcely functional, and are elongated with time, is simply wrong: facts do not support it.
First, it isn't my theory; it reflects the consensus of those who know more about protein evolution than either of us. Secondly, it is consistent with the statistics relating the mean length of proteins to their evolutionary age. If you don't mind, I would appreciate some information about the flavour of ID that you prefer. Guided evolution, which accepts universal common decent, speciation, etc., over billions of years, but "the designer" is required to tweak the genome every time when some new function is to evolve?
It seems that either the designer or unguided evolution added proteins which are shorter as time passes and remain shorter. How do you explain that? O have given an explanation. What is yours?
Your answer is a non-explanation. We still don't know why "the designer" behaves in this fashion. My explanation is simple: I reject your assertion that protein length can't evolve.
So, why are mammal de novo genes less complex that vertebrate genes?
The first vertebrates are more than twice as old as the first mammals. When the mammalian de novo genes arose, the vertebrate ones had already been evolving for 300 million years.Piotr
May 2, 2014
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jerry:
So far I haven’t seen too many explanations but they should come if they exist.
An easy prediction. You will not see them, because they don't exist.gpuccio
May 2, 2014
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Piotr: Another example on which you could reflect. RAG1 is an important protein which effects DNA recombimnation in the adaptive immune system. The adaptive immune system is foung only in vertebrates, and it originated in jawed fish approximately 500 million years ago. That's when the RAG1 protein appears. Now, i did a simple blast of the protein in zebrafish and the protein in humans. The result: Protein length: Zebrafish: 1057 AAs Human: 1043 AAs Score 1249 bits(3231) Expect 0.0 Identities: 632/1067(59%) Positives: 786/1067(73%) The final two thirds of the two molecules are practically identical. Now, if this important protein appeared in jawed fish, and if it retains practically the same length and sequence in humans, it is obvious that it had more or less the same length and sequence when it appeared in the first jawed fish. IOWs, when it was a de novo gene. How do you explain that?gpuccio
May 2, 2014
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A large percentage of these questions about de novo genes will be answered in the next 15-20 years as more genomes get sequenced. Something does not come from nothing without leaving a trail in the genomes of related species. If the trail is there then most if not all the history of a gene will be available. If it is not there, then that will be a major mystery for those who propose naturalistic evolution. What may be of interest now is just how many genes have a known history as to how they developed. I am not talking about speculation or just told stories but genomic forensic evidence. Which one of the 50 engines of variation did each gene begin with, how did it change over time, why did some populations get the functional sequence while others did not. Does any of it challenge Axe and Durston's ideas? So far I haven't seen too many explanations but they should come if they exist. What will probably dominate biology is not de novo genes but the origin of the control mechanism in the genome. Control mechanisms in the human genome are apparently incredibly more complex than its nearest so called cousin, the chimp. How did these networks arise? Must have happened somewhere in Africa because all were established when humans left Africa. And why didn't this process spawn many other species with equal or slightly less complex control mechanisms. A mystery!jerry
May 2, 2014
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Piotr: a) In Durston's paper, the minimum functional complexity found is 46 bits, for Ankyrin, which is 33 AAs long. All proteins longer than 65 AAs have more than 150 bits of functional information (except one which is 123 bits). Unless de novo genes are completely different from all other functional proteins we know of, their functional complexity cannot be explained by random variation. b) Proteins are longer when they are older. But that's not because they start short and gradually become longer. Older proteins start longer, and more recent proteins start shorter. And remain shorter. As I have shown you with the example of ATP synthase, proteins do not grow in length and complexity with time. I could give many other examples. Therefore, the reasonable explanation for shorter proteins in more recent history is that different kinds of proteins and of functions become necessary at different steps of evolution. This is not ad hoc, it is simply what facts suggest. Your theory, that proteins start short and scarcely functional, and are elongated with time, is simply wrong: facts do not support it. c) You ask: "Let’s try again: what prevented the designer from adding something “more basic” to a genome in recent times?" It seems that either the designer or unguided evolution added proteins which are shorter as time passes and remain shorter. How do you explain that? O have given an explanation. What is yours? d) You ask: "My question was not about genes with three-billion-year-old pedigrees (we don’t call them de novo genes) but about recently formed orphan genes. " But the point is that the "shorter" rule is equally valid for old pedigrees. In the paper, you can see that the mean prtein length in vertebrates is 624 AAs, while in mammals it is 329. That is a big difference. How do you explain it? You cannot evade the question just saying that "we dn't call them de novo genes". As I have said, each new gene is a de novo gene when it appears. So, why are mammal de novo genes less complex that vertebrate genes?gpuccio
May 2, 2014
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Piotr- I don't care what you do. I am positive that you will never provide any evidence for unguided evolution producing de novo genes. And that is all that counts. IOW you are the peanut galleryJoe
May 2, 2014
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@Joe Excuse me if I ignore your peanut gallery heckling.Piotr
May 2, 2014
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Piotr- your entire position is completely ad hoc. So perhaps you should just stop and face the music.Joe
May 2, 2014
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What about primate de novo genes? It is true that they are rather short proteins, but not so shoort: The mean length is 100 AAs, with a median og 90 and a SD of 53. That means that many of them are definitely longer than 100 AAs.
It means that some of them are somewhat longer, but nowhere near the average length of older proteins. Those that are specific to Eukarya, for example, have lengths in the 500-600 aa range (and some may be twice or more as long). And note that you are talking about primate TRGs now. They are in fact quite old (~ 65 million years).
If you read the paper, you will see that ol[d]er proteins are longer throughout natural history.
Precisely. Why should that be the case?
The reason why more recent proteins become shorter in time is probably another one: they have different types of functions, more regulatory and less basic.
This is completely ad hoc. Let's try again: what prevented the designer from adding something "more basic" to a genome in recent times?
You ask: “What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long -- de novo?” Nothing. Indeed, he has done that: at OOL, and in the first phases of protein evolution. ATP synthase is a good example. Remember, ATP synthase, like any new basic protein, was a de novo gene when it first appeared.
This is a red herring. My question was not about genes with three-billion-year-old pedigrees (we don't call them de novo genes) but about recently formed orphan genes. Why can't their products be anywhere as complex as those of phylogenetically old genes (such as the ATP family)?Piotr
May 2, 2014
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Evolve:
The author wants to hide the fact that new genes have been shown to arise from ancestral non-coding DNA by the well-understood process of mutation.
LoL! Being well understood doesn't make it unguided. The processes that run my computer are well understood. The processes that run my car are well understood.Joe
May 2, 2014
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Who cares about proteins with a length shorter than 100AA? Most proteins are much longer than that. And there is no way to get longer proteins once you have one.
What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long de novo?
Nothing and obviously it happened at the OoL- the intervention event. However now there isn't any intervention now. Organisms have to rely on their built-in responses to environmental cues- most of which occur within the immune system- something else that unguided evolution cannot explain.Joe
May 2, 2014
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Piotr: a) It is complex functional information which cannot be generated randomly. Simple functions can emerge randomly, but they do not lead to complex functions. Known example of microevolution are 1 -2 AAs (less than nine bits). I have proposed a threshold of 150 bits of functional information for design inference in biological objects. Behe and Axe, from observed models, stick to 3 - 5 AAs (which would be less than 22 bits). Many proteins are beyond the 500 bit threshold (Dembski's UPB), as you can see from Durston's paper. b) What about primate de novo genes? It is true that they are rather short proteins, but not so shoort: The mean length is 100 AAs, with a median og 90 and a SD of 53. That means that many of them are definitely longer than 100 AAs. If you read the paper, you will see that oler proteins are longer throughout natural history. I have recently pointed to ATP synthase, which is extremely long and complex just from the beginning. Subunit beta shows more than 300 AA identities between E. coli and humans. It is not an old protein which became complex in time. It is an old protein which was complex when it started. The reason why more recent proteins become shorter in time is probably another one: they have different types of functions, more regulatory and less basic. b) It does requires a design intervention for any protein gene (or any other digital sequence) to acquire more than a definite threshold of complex functional information (let's say more than 150 bits, 35 fixed AAs, to stay conservative). c) Any functionality will do, but to be selected a functionality must confer a reproductive advantage. Let's say that any naturally selectable functionality will do. And, if we know the function and its molecular basis, we can compute the functional complexity for that specific function. And simple, stepwise functions, if and when they exist, do not build complex functions, except in the imagination of neo darwinists (can I use the word?). d) Why do you say that the function of de novo genes would be "marginal". On what empirical basis? The functions of the 6 of them which are known are not marginal. Primates are different from other mammals, aren't they? But they share all basic genes, like ATP synthase, with older species, even with bacteria. Most researchers agree that the difference in higher species is mainly regulatory. Would you call that difference "marginal"? e) You ask: "What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long de novo?" Nothing. Indeed, he has done that: at OOL, and in the first phases of protein evolution. ATP synthase is a good example. Remember, ATP synthase, like any new basic protein, was a de novo gene when it first appeared. I hope I have been concise enough. When I give only a short comment, you accuse me of "rigmarole of lies", When I try to give you details to answer a specific question which I have been debating for years, you accuse me of Gish gallop. I can be as short or as long as you like. It only depends on your questions and your interest.gpuccio
May 2, 2014
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Short comments to my long posts. But it’s better than nothing. I wasn't asking for much. For starters, let's discuss something very specific. Not "digital functionally specified complex information" linked to intelligent design "with 100% specificity", but plain old "function" in the sense that biologists attach to this word. Why do you think it requires a miracle (or intervention by supernatural forces) for a protein sequence shorter than 100 amino acids to acquire some sort of function? Mind you -- any functionality will do. It doesn't have to be noble and refined to be promoted by positive selection. You say it's against all probabilistic odds. How on earth do you know? And while we are at it: why are all de novo genes like that? Why (if they encode for a protein) the product is short and its function (if identifiable at all in the first place) is rather marginal? What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains -- hundreds or thousand aa long de novo? I asked Joe this question and he evaded answering it. Perhaps you have a good answer. But please make it concise. I do not like the Gish gallop.Piotr
May 2, 2014
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Piotr: Short comments to my long posts. But it's better than nothing. I have been defining function and functional complexity for years here. I have also defined in detail my specific concept of functional complexity, dFSCI (digital functionally specified complex information). And I have shown many times why dFSCI can be empirically linked to design with 100% specificity, and therefore used as an extremely good tool for design inference. I am preparing an OP on the subject, but I need some more time to finish it. I have also debated that on other non design blogs, like TSZ (The Skeptical Zone). There was also a long challenge about dFSCI between me and those at TSZ. However, I will try to give you some inputs from recent posts of mine on the subject: 1) From a debate with Jerad two years ago:
So, in a nutshell: a) Design is the act by which conscious intelligent beings, such as humans, represent some intelligent form and purposefully output that form into some material system. We call the conscious intelligent being “designer”, and the act by which the conscious representation “models” the material system “design”. We call the material system, after the design, a “designed object”. b) Some designed objects (not all) have a specific property, objectively verifiable, that we call “CSI”: that is, they bear meaningful information (the design), and that meaningful information is complex. c) A specific form of CSI is what I call “dFSCI”, that is CSI that is both digital and functionally specified. Let me confine the discourse to this form, for the moment. d) For all the objects we can observe in our reality, and whose origin is known, it can be always verified that any object exhibiting dFSCI has been designed by a conscious intelligent being (in practice, some human). No counterexample exists. e) Of all the objects we can observe in our reality, except human artifacts, only one category, whose origin is at least controversial, exhibits dFSCI. That category is biological objects. f) It is perfectly reasonable, therefore, to hypothesize that biological objects are designed. That naturally brings to the question of what kind of conscious intelligent agent designed them, but that question in no way makes the inference less valid. g) If you and your similar cannot even accept the above inference as a valid scientific hypothesis, and indeed as the best explanation at present for biological information, I can only say that you have a methodological problem, and that you are in principle committed to a specific world view and ideology, probably materialistic reductionism, or scientism (which are more or less the same thing). No problem, anybody is free to believe anything. But I cannot count on your scientific objectivity.
From the same thread:
The point is not that humans are the only known source of dFSCI (which is empirically true). The point is that we are witnesses of the process of design, especially when we ourselves design something. So, we know intuitively that, in the process of design, a mental representation involving meaning and purpose is the true origin of the oordered output that shapes the final physical system. It can be a cognitive representation, or some artistic intuition, or anything else, but the point is always the same: we have to consciously represent what we want to achieve, and how to achieve it, before using our physical body to shape the physical system that will be the “storage tool” of our representations. It’s always that way: Meaning and purpose are always the source of design. We have to have a desire, and to know how to satisfy it. So, in the end, the simple truth is: any being who can represent, understand and have intent can be a designer. It is not important that it be a human. As the example of aliens clearly shows. So the problem is, are humans the only beings who can represent, understand and have intent? Well, the question is at least open to discussion. A very big discussion, I would say. Another common objection is that the designer must have access to some physical tool to design. Indeed, we conceive design in our consciousness, but we design through our bodies. Now, I will happily admit that the designer needs to manipulate matter to design biological information. And yet, if we exclude the hypothesis of aliens, I will also admit that the most likely scenario for the biological designer(s) is that he is not a physical being with a body. So, what about that? Again, are we really sure that any conscious being must have a physical body? I would only say that we know nothing about the final nature of consciousness. If we want to stay empirical, we can only treat it as an objective reality that we perceive subjectively (in ourselves), or infer (quite reasonably) in other beings. So, the point is, if it is true (and it is true!) that consciousness cannot be explained in terms of objective aggregations of matter, we must still describe our reality as a continuos interaction between our consciousness and our physical body. That interaction is absolutely real, even if we have no idea of what our consciousness is. Perception and will are the obvious input and output of that interaction. So, there is no doubt that our conscious representations do manipulate the physical reality that is our body. (I will not even consider here the squalid view of reductionists, that cosnciousness is only a byproduct of the physical working of the brain, and that no free will exists, and so on. It is a world view that is not only foolish, but completely unsupported by any serious consideration, either scientific or philosophical). So, it is a fact that our conscious representations are influenced and do influence our physical body. How does that happen? We don’t know, but here we have something very similar to what the biological designer does with living beings: he influences them starting from his conscious representations. What we daily do with our brains, he can do with biological beings. Is that so strange? Not to me. It has never been strange for billions of intelligent human beings who have lived and still live on our planet, and who have intelligently, consciously, seriously believed in the existence of some form of spiritual intelligence that can interact with our world, and does exactly that. I do believe that, like them, like many, and I will not accept that my worldview, that I find simple, beautiful and deeply satisfying both for my intellect and for my heart, should be considered less “scientific” than anyone else’s only because it is different from the shared dogma of our generation. OK, maybe I have said too much, but sometimes one just needs to state things as they are.
You can also look at my OP about design definition, here: https://uncommondescent.com/intelligent-design/defining-design/ Or, for more detail look at my posts 680, 682, 684, 685, 686, 687, 688, 689, 691, 693, 694, 695 (and many others following and analyzing TSZ's objections) here: https://uncommondescent.com/design-inference/it-seems-that-tsz-objector-to-design-af-insists-on-the-long-since-corrected-canard-that-design-is-a-default-inference/#comment-434682 For an example of computation of functional information in protein families, please read the fundamental Durston paper: "Measuring the functional sequence complexity of proteins" http://www.tbiomed.com/content/pdf/1742-4682-4-47.pdf If you are interested, I am fully available to discuss any specific aspect of the issue again with you. Whenever you like. Finally, my simple idea is that functions related to the neural system, or the immune system, or the reproductive system, are "high level" functions. For example, the de novo genes identified in drosophila were expressed in the testis. The idea is that de novo genes active in the neural system, the immune system and the testis are prominent in recent speciation. There are data suggesting that, IMO, also in the recent FANTOM5 papers. If I have time, I will try to comment on them.gpuccio
May 2, 2014
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None of these three mechanisms has any potential to generate functional protein information, if unguided. All of them require a design intervention to happen as we observe them, with the functional results we observe. Define "function" and explain to me why it's impossible to acquire a function without divine disine design intervention. As you can see, these seem rather noble, refined functions. They are just "functions" of sorts. I fail to see what's noble or refined about them.Piotr
May 2, 2014
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Piotr and all: Let me hijack again a few facts. The paper you quoted derives its facts mainly from another important paper: "Origin of Primate Orphan Genes: A Comparative Genomics Approach" http://mbe.oxfordjournals.org/content/26/3/603.full.pdf which is very good, and that I invite everybosy here to read, because it is the kind of paper that hijackers like me do prefer: many facts, and mainly honest and interesting empirical interpretations. Some examples of honest and interesting interpretations:
We have determined that primate orphan genes evolve about four times faster than the average gene. Such rapid evolutionary rates may be related to relaxed functional constraints on proteins with newly acquired functions and/or to positive selection linked to adaptive evolution
Emphasis mine.
It has recently been argued that most of the annotated human orphan proteins are likely to be spurious ORFs that are not functional (Clamp et al. 2007). Here we only considered human gene products that showed significant similarity to putative macaque and chimpanzee proteins and, with this data set, we reached quite different conclusions regarding the possible functionality of orphan genes.
And many other good things. Is there darwinist propaganda here? Well, just a little bit, at the end:
These studies have revealed that a much larger fraction of the genome than previously thought is found in primary transcripts, potentially increasing the opportunities for new gene functions to arise. Short ORFs present in such transcripts could occasionally be translated into new peptides, which would then be tested by natural selection. If advantageous, the new function would be retained and continue to evolve. We hope our results will encourage further studies on the evolutionary and functional implications of newly formed genes.
OK, this is propaganda, but it is expressed with great caution (note the many semantic tags of wishful thinking), and it is at the end, completely separated from the facts in the paper, completely independent from the interesting conclusions in the paper. IOWs, just a due homage to the party line. Now, let's go to the interesting facts, and do a little criminal hijacking. A very important part are the results in Table 3 about the 270 primate de novo genes they studied: Categories of Primate Orphan Genes: Mechanism of Formation of Primate Orphan Gene: Gene duplication: 66 (24%) Exaptation from TEs: 142 (53%) De novo formation from noncoding regions: 15 (5.5%) Unknown: 47 (17%) This is really interesting. De novo formation is an inportant and well documented mechanism (5.5%), as is the traditional model of gene duplication and variation (24%), but the main mechanism, by far, seems to be the one I love most: transposons (53%). The important points: a) None of these three mechanisms has any potential to generate functional protein information, if unguided. All of them require a design intervention to happen as we observe them, with the functional results we observe. b) Transposon variation should be the least related to function, the most devastating. Instead, it is exactly the one which generates most function. c) The 270 new genes have documented function in 6 cases: - dermcidin, encoding a peptide secreted in sweat glands with antimicrobial activity, which has also been reported to be involved in neural survival and cancer - a role in immune response (minor histocompatibility protein HB-1, which is able to stimulate T-cell responses) - the SPHAR gene (S-phase response), involved in the regulation of DNA synthesis - two more genes, FAM9B and FAM9C, exclusively expressed in testis, have been suggested to play roles in mediating recombination during meiosis - one protein from the primate specific morpheus gene family has been shown to locate in the nuclear pore complex As you can see, these seem rather noble, refined functions. According to the facts presented by the authors, the properties of the other 264 de novo genes are similar to those of the 6 for which a function has been shown. That is a good point for the possible functionality of all or most of them.gpuccio
May 2, 2014
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Piotr:
Have you got a creationist/designist explanation of the fact that orphan genes in humans (similarly to those in other species) don’t encode for complex proteins, that they are all single-copy genes...
Are these "young orphan genes" and how would you know? Is it because they are short and don't code for anything all that complex? Because there are no duplicates of them?
For example, if you could show me a young orphan gene that encodes for a large and highly complex multi-domain protein involved in some really important interactions, I’d agree that the spontaneous rise of such a structure by accident is not a satisfactory explanation.
If shown such an orphan gene, would you say it could not be young, because young orphan genes just don't encode for large and highly complex multi-domain proteina involved in really important interactions and must have duplicate copies? Why are numerous short functional orphan genes more probable than a single one that codes for a complex protein?Mung
May 1, 2014
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Joe:
Mung, Nice quote mine of Spetner. The part you quoted has nothing to do with what I am saying. Spetner also talks about long term changes, Mung.
Sorry, but that just happened to be where I had left off reading for the night. The following paragraph in the book is just a bunch of handwaving.
It’s as if y6ou have turned into an evo
It's as if I've made the same arguments against young earth creationism ever sine I've been here. They can't make up their minds whether they are pro or anti evolution. Even you seem to be conflicted. Is God creating new orphan genes, as Jehu thinks, or do they arise as a matter pre-programming through non-random evolution? What's the difference between God the programmer and God the clockmaker who winds things up and then they run on their own?Mung
May 1, 2014
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Quote mining. The author conveniently left out the following sentences from Carl Zimmer's article hoping that most readers won't notice it: "One reason it no longer seems so improbable is that Dr. Begun and other researchers have documented the step-by-step process by which a new gene can come into existence. In many species, ours included, protein-coding genes make up a tiny portion of the genome. New genes can emerge from the vast expanse of noncoding DNA. The first step is for a tiny bit of DNA to mutate into what scientists call a “start sequence.” All protein-coding genes have start sequences, which enable cells to recognize where genes begin. Once a cell recognizes the start of a gene, it can make a copy of the gene’s DNA. It can then use that copy as a guide for building a protein. The new protein may turn out to be toxic, or it may serve no purpose. But once it emerges, new mutations to the new gene may make it more useful. “Once they’re produced, there’s an opportunity for natural selection to sculpt them,” said Aoife McLysaght, a geneticist at Trinity College Dublin. Dr. Begun and his colleagues are now getting a look at these early stages in the birth of de novo genes. They can do so by looking for such genes in different populations of a species of the fruit fly Drosophila melanogaster." The author wants to hide the fact that new genes have been shown to arise from ancestral non-coding DNA by the well-understood process of mutation.Evolve
May 1, 2014
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Piotr:
If you mean that there is no such mechanism known to you, I’m prepared to believe you. Perhaps hou’ve never heard of domain duplication, insertion, gene fusion, recruitment of transposable elements, etc.
Please demonstrate that any of those can add to the AA length of an existing protein. Next tell us how it was determoned those changes are accidental. As I said you have no evidence that gene dupication is accidental. As I said that all goes back to the OoL- stay focused, indeed. And again there isn't enough time for chance to do it, Piotr. You are asking way to much of luck, and that ain't science.Joe
May 1, 2014
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Piotr:
Shall I stop taking you seriously before we actually discuss anything?
Your choice.
I gave you a link to a review article by highly respected experts on orphan genes, published in one of the best science journals, and you dismiss it off-hand as “darwinist propaganda” and a rigmarole of lies.
First of all, I already knew that paper. Second, my comment about the propaganda was mainly referred to your statements, rather than specifically to that paper. Third, that paper contains however a lot of darwinist propaganda, especially in the section "Emergence of protein structure", even if it is expressed with some cautious intelligence. Fourth, the fact that researchers can do good work and be "highly respected experts" in their field is not in discussion, and has almost nothing to do with what we are discussing here. My point here, the point of many in ID, is that our scientific community has been experiencing a strong cognitive bias, in the last decades, in favor of a theory completely unsupported by facts, and logically inconsistent. This is a confrontation of paradigms, not of individuals. So, I will not accept anything here because of authority, not even from my side. And what are the "lies" you refer to? I stated: "Unfortunately, nothing of that is true or supported by facts." I was referring to the following statements made by you: a) "the accidental formation of a new “RNA gene”, complete with regulatory elements, is not at all unlikely." Based on what facts? That new genes (DNA genes I suppose, but transcribed) happens? Of course it happens. That is obvious. And where is the evidence that it is "accidental"? The whole point of ID is that functional genes cannot emerge by chance. And even if transcribed genes emerged by chance, they still would not be translated, and therefore would not be visible by NS. Where are the evidences that cells are repleted with non functional transcribed and translated genes, on whom NS can act? They are nowhere to be seen. b) "Again, in most cases it will be non-coding RNA which may or may not become co-opted for doing something useful.". Based on what? Again, I agree that new genes come often from non coding DNA, but how does that DNA become apt to be "co-opted", IOWs functional, against all probabilistic laws? No facts, no consistency. c) "In extremely rare cases it may be translated into a protein (short, simple and relatively unstructured in the case of young genes, which doesn’t rule out certain kinds of functionality)." Again, where are the facts that support this bizarre statements? This is complete mythology. Then I stated "However, you certainly believe those things in good faith.", which I hope is not a lie, and gave you a link to some posts of mine which go in greater details. Where is the "rigmarole of lies"? Finally, I use propaganda to mean exactly that: propaganda. Concepts enforced to defend a wrong theory, without any rational and empirical support, are propaganda in my world. And I use the term "darwinism" for brevity, usually meaning neo darwinism, the modern synthesis, classical darwinism a la Dawkins. No agit prop application at all. When I want to be more precise, I refer in general to "non design theories of biological information". I have been debating here for years the scientific reasons why none of those theories makes sense. I have given you a link to more detailed posts of mine. I don't think it is fair on your part to label me in ways that have nothing to do with what I defend here. But again, it is your choice. Then I find this bizarre statement: "How can you, on the one hand, call someone’s results not true and unsupported by facts, and at the same time hijack them for your own purposes? It simply makes no sense." I hate to remind you that there is a great difference between facts and their interpretation, in science. I appreciate facts, and those researchers who provide good facts. I feel in no way obliged to share their interpretation of those facts, if I believe that it is biased or simply wrong. Hijacking facts is a crime, now? Are you really serious? In another post, you say: "The null hypothesis is the default position. " No. There is no "default" position in science. The null hypothesis is the hypothesis that the observed effect is due to chance. It is considered only to the purpose that its probability may be assessed. It's that probability which will tell us if it is reasonable or not to reject the null hypothesis. You may be aware that neo darwinism avoids accurately the computation of real probabilities. That is the weapon of ID. Well, you should be satisfied. Now you can stop taking me seriously after I have actually discussed something. :)gpuccio
May 1, 2014
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Piotr,
I prefer to stay focussed especially if straying off topic could be employed as an evasive tactic.
Well that's exactly the point, I was making. The origin of the system that you take for granted in order to make your case is not off topic if your professed conclusion is that life is the result of a purely material process. Life is wholly dependent on an irreducibly complex system that cannot come into being by a stepwise process. Life is either the product of an inconceivable miracle of chance, or it is designed. And while the evidence surrounding a chance origin is less than zero, the physical evidence leading to a designed origin is both intractable and universal. If you are expecting ID proponents to ignore this fact so that our opponents aren't bothered by it, then you simply ask too much - certainly more than you are willing to give.Upright BiPed
May 1, 2014
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Upright Biped: They can’t “arise and evolve” without the irreducible complex system that precedes them. Still, the topic under discussion is the origin of orphan genes themselves, not the prehistory of the whole milieu in which they exist (or the origin of life, or the origin of the Universe, or my world-outlook). I'm willing to discuss anything on suitable occasions, but I prefer to stay focussed especially if straying off topic could be employed as an evasive tactic.Piotr
May 1, 2014
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Hello Piotr
The issue at hand is not what happens to orphan genes and their products once they arise and start evolving, but whether they can arise by chance in the first place.
They can't "arise and evolve" without the irreducible complex system that precedes them.
Duplication, let alone the origin of life, are separate topics.
If it is argued by materialists that a life can be fully explained by unguided material processes (as is the case) ... yet unguided material processes cannot explain the material conditions required for life to exist - then it is not a wholly "separate topic". If materialists would like to reformulate their public proclamations that life is the result of a purely unguided material process, and amend it to say that there are important observations within the evolution of life that are explicable by purely material means - then we (generally, as a group) would have no problem with that position. It is the same one that ID proponents hold.
We are talking about the origin of orphan genes at the moment, so please let’s stay focussed.
If you are sensing resistance, perhaps you should realize that most ID proponents understand this to be a cop out. You are here clearly arguing that life is the product of materialial processes. So the obligatory "Let's not talk about the evidence that materialism fails to address" is hardly sufficient to the ultimate question you are attempting to support. Obviously, there is nothing improper about limiting a discussion to a particular topic. There are many here that can (and will) address the mechanism(s) of the origin of orphan genes. Perhaps it would serve your purposes better to not merely say that the origin of living systems is simply "a separate topic", but to acknowledge the evidence of design regarding origins, and its potential implications in the topic you wish to discuss. Such balance and discipline has appeared on these pages before, and typically results in a much more fruitful conversation.Upright BiPed
May 1, 2014
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Also yours has the issue of once you have a functioning short protein there isn’t any known mechanism for adding to that sequence in such a way as to produce a totally new function with a longer chain. If you mean that there is no such mechanism known to you, I'm prepared to believe you. Perhaps hou've never heard of domain duplication, insertion, gene fusion, recruitment of transposable elements, etc. All that stuff, however, is beside the point. The issue at hand is not what happens to orphan genes and their products once they arise and start evolving, but whether they can arise by chance in the first place. Duplication, let alone the origin of life, are separate topics. We are talking about the origin of orphan genes at the moment, so please let's stay focussed. Have you got a creationist/designist explanation of the fact that orphan genes in humans (similarly to those in other species) don't encode for complex proteins, that they are all single-copy genes, and that despite being specifically human, they correspond to non-translatable orthologous sequences in chimps and orangutans? Why should the designer have limited her creative freedom in this way?Piotr
May 1, 2014
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