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Author | Topic: The origin of new genes | |||||||||||||||||||||||||||||||||||||||||||
bernd Member (Idle past 4001 days) Posts: 95 From: Munich,Germany Joined: |
In recent threads the role of mutation for evolutionary processes has been the point of issue. One side seems to claim that the phenotypic and genetic diversity of sexual reproducing organism can be explained without mutation - all observed “novel” traits are viewed simply as the result of a new combination of pre-existing alleles.
It might therefore be interesting to discuss the molecular processes which generate new genes.A good introduction offers the following review published in Nature Reviews Genetics 4, 865-875 (2003), which describes the currently known mechanism of novel gene formation:
In order to keep the discussion focused I would propose to concentrate on “jingwei” a recently (~ 2.5 million years BP) evolved gene in Drosophila, which has been formed by the combination of exon shuffling, retroposition and gene duplication. The article provides a short overview:
In the early 1990s, the first young gene to be described was jingwei in a group of African Drosophila species32. It provided enough details for the molecular mechanism underlying its origination to be deduced. A portion of jingwei was found to be a homologue of the Adh gene that encodes alcohol dehydrogenase98 and was later characterized as a retrosequence of Adh99. Further population genetic, molecular biological and comparative phylogenetic analyses showed it to be a new processed functional gene that originated around 2 million years ago in the common ancestor of two African Drosophila species, Drosophila yakuba and Drosophila teissieri. In the ancestral species, there were two single copy genes, yellow-emperor (ymp) and Adh. yellow-emperor was duplicated into two copies: one also called yellow-emperor and the other called yande (ynd)100,101.Whereas yellow-emperor maintained its original functions, yande was further involved in the origin of jingwei. In the short time before the speciation event, Adh mRNA retroposed into the third intron of yande as a fused exon and recombined with the first three yande exons. This formed jingwei, which is a gene that is translated into a chimeric protein. The funtion of jingwei has been described in the following article . The abstract reads:
The mechanism by which protein functional diversity expands is an important evolutionary issue. Studies of recently evolved chimeric genes permit direct investigation of the origin of new protein functions before they become obscured by subsequent evolution. Found in several African Drosophila species, jingwei (jgw), a recently evolved gene with a domain derived from the still extant short-chain alcohol dehydrogenase (ADH) through retroposition, provides an opportunity to examine this previously undescribed process directly. We expressed JGW proteins in a microbial expression system and, after purification, investigated their enzymatic properties. We found that, unexpectedly, positive Darwinian selection for amino acid replacements outside the active site of JGW produced a novel dehydrogenase with altered substrate specificity compared with the ancestral ADH. Instead of detoxifying and assimilating ethanol like its Adh parental gene, we observe that JGW efficiently utilizes long-chain primary alcohols found in hormone and pheromone metabolism. These data suggest that protein functional diversity can expand rapidly under the joint forces of exon shuffling, gene duplication, and natural selection.
Taken together I claim that we look at an example that mutation created a novel, useful gene - which seems to me difficult to reconcile with the above mentioned view which implies that no natural process is able to create new alleles, let alone new genes. -Bernd Edited by bernd, : Spelling correction Edited by bernd, : insertion of "which implies" in last sentence
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AdminNosy Administrator Posts: 4754 From: Vancouver, BC, Canada Joined: |
Thread moved here from the Proposed New Topics forum.
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Faith  Suspended Member (Idle past 1465 days) Posts: 35298 From: Nevada, USA Joined: |
Nobody has doubted that new alleles, genes, are formed by mutation FROM TIME TO TIME. At least in bacteria and perhaps fruit flies this has been shown. It has NOT been actually demonstrated in mammals which is where most of the discussion is. All the mechanisms you have listed may in fact bring about a new gene / allele, but at what rate? How often is it useful or does it actually contribute to variation? Considering how many alleles already exist in most populations of sexually reproducing animalia how on earth would you know if the occasional mutation contributed anything whatever to the processes that lead to variation, as opposed to the usual shuffling of gene frequencies among those already in existence?
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NosyNed Member Posts: 9003 From: Canada Joined: |
There have been specific studies referenced which show that there are billions of mutations in the human gene pool in each generation. Billions with a "B".
You have ignored what you've been told.
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Archer Opteryx Member (Idle past 3618 days) Posts: 1811 From: East Asia Joined: |
Many thanks to bernd for taking the time to present this. A cogent presentation supported by authoritative research.
I look forward to learning more about this. Archer All species are transitional.
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sidelined Member (Idle past 5928 days) Posts: 3435 From: Edmonton Alberta Canada Joined: |
Faith
Nobody has doubted that new alleles, genes, are formed by mutation FROM TIME TO TIME. At least in bacteria and perhaps fruit flies this has been shown. It has NOT been actually demonstrated in mammals which is where most of the discussion is You must be living in the dark ages. You are aware that cancer is caused by mutations don't you? Being that it is the second leading cause of death in human mammalsthen we can hardly state that it has not been demonstrated to be shown. It is not merely shown it is demonstratably widespread.
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Faith  Suspended Member (Idle past 1465 days) Posts: 35298 From: Nevada, USA Joined: |
Nobody has doubted that new alleles, genes, are formed by mutation FROM TIME TO TIME. At least in bacteria and perhaps fruit flies this has been shown. It has NOT been actually demonstrated in mammals which is where most of the discussion is You must be living in the dark ages. You are aware that cancer is caused by mutations don't you? Being that it is the second leading cause of death in human mammalsthen we can hardly state that it has not been demonstrated to be shown. It is not merely shown it is demonstratably widespread. Oh yes, I certainly know that DISEASES are caused by mutations. Diseases and deformities and miseries galore are caused by mutations. This is one of the reasons why mutations hardly seem like an engine that could power life at all. Again, of course mutations OCCUR, the doubt is whether they could possibly do what the ToE requires them to do, and I have not seen any actual facts that demonstrate that they could or do, merely speculations and assumptions.
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Faith  Suspended Member (Idle past 1465 days) Posts: 35298 From: Nevada, USA Joined: |
There have been specific studies referenced which show that there are billions of mutations in the human gene pool in each generation. Billions with a "B". You have ignored what you've been told. Oh I have not ignored this at all. It is part of my argument that mutations can't do what the ToE requires them to do. I don't know that "billions" of mutations have been "shown" to exist in the human gene pool, since claims about mutations are often asserted but rarely actually demonstrated, but perhaps there are that many; I know there are a lot. However, most of them wipe out useful alleles apparently, since they have no function, or bring about disease, and some minuscule number can said VERY IFFILY to confer a benefit, usually in exchange for a downside. Not the sort of mechanism that could power evolution. Edited by Faith, : No reason given.
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Dr Adequate Member (Idle past 305 days) Posts: 16113 Joined:
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Oh I have not ignored this at all. It is part of my argument that mutations can't do what the ToE requires them to do. I don't know that "billions" of mutations have been "shown" to exist in the human gene pool, since claims about mutations are often asserted but rarely actually demonstrated, but perhaps there are that many; I know there are a lot. However, most of them wipe out useful alleles apparently, since they have no function, or bring about disease, and some minuscule number can said VERY IFFILY to confer a benefit, usually in exchange for a downside. Not the sort of mechanism that could power evolution. There should have been some reasoning between the penultimate and final sentence. --- One nice example of a beneficial mutation in mammals is the origin of "three-color vision" in Old World primates, which involved duplication of a gene followed by mutation of one of the copies. Hence, whereas most mammals see only in "two-color" vision, with "red" and "blue" receptors, we and our cousins also have a "green" receptor which is almost, but not quite, identical to the "red" one. Interestingly, reptiles see in seven colors (imagine how expensive a TV would be if you were a lizard). But the primitive mammal-like reptiles, you wil recall, were nocturnal, and developed rods at the expense of cones. For our diurnal fruit-eating ancestors, however, the ability to tell red from green is clearly an adaptive trait. Here's a paper on the genetics of vision in primates.
Nathans, J. The Evolution and Physiology of Human Color Vision, Neuron, Vol. 24, 299-312, October, 1999
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NosyNed Member Posts: 9003 From: Canada Joined:
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See:
Some women may see 100 million colors, thanks to their genes Some women posses an addition kind of cone. Perhaps not by coincidence on studied is an interior designer. There maybe 2 or 3 % of women with this.
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Faith  Suspended Member (Idle past 1465 days) Posts: 35298 From: Nevada, USA Joined: |
One nice example of a beneficial mutation in mammals is the origin of "three-color vision" in Old World primates, which involved duplication of a gene followed by mutation of one of the copies. I would really like to know how you think you KNOW that a mutation was involved. This is all typical speculative thinking. I can't look at the link because my computer doesn't like switching websites these days, and it's probably more time-consuming technicalities than I'm up for anyway, which I'd appreciate your explaining in your own words.
Hence, whereas most mammals see only in "two-color" vision, with "red" and "blue" receptors, we and our cousins also have a "green" receptor which is almost, but not quite, identical to the "red" one. Design differences explain this just fine; no need to postulate mutation from one to the other.
Interestingly, reptiles see in seven colors (imagine how expensive a TV would be if you were a lizard). But the primitive mammal-like reptiles, you wil recall, were nocturnal, and developed rods at the expense of cones. Design difference explain all this just fine; no need to postulate mutation from one to another.
For our diurnal fruit-eating ancestors, however, the ability to tell red from green is clearly an adaptive trait. Design, etc.
Here's a paper on the genetics of vision in primates. Please explain briefly and clearly in your own words how mutation is *known* to have anything to do with these differences between creatures. Thank you.
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bernd Member (Idle past 4001 days) Posts: 95 From: Munich,Germany Joined: |
Hello Faith,
you seem to accept that new genes are formed by mutation in bacteria and drosophila, but you ask for evidence that the same holds true for mammals. I would propose to have a closer look at the review I already provided in my opening post, specially at table 2 which lists 22 examples of novel genes within drosophila, primates, rodents, fish, plants and protozoa (each with references to the relevant primary literature). You’ll find 11 examples of mammalian genes, one - named FOXP2 - is a transcription factor which controls language and speech related functions in homo sapiens. Another example of an "useful" mammalian gene would be GLUD2, a gene, which probably affects higher cognitive functions. It has been formed by retrotransposition from the household gene GLUD1 in the hominoid line about 23 million years BP. It is expressed in human nerve and testis tissue and seems to positively influence cognitive functions by enhancing the flux of a neurotransmiter. To answer your last question
faith writes:
Please read the chapter “Frequency of origin of new genes” in the above mentioned article . Whereas the exact rate of novel gene formation is yet not known, it is clear that processes like exon shuffling ore retrotransposition have shaped the genome of the eukaryotes. To give an example: at least two independent studies - a detailed structural analysis of protein super families and the observed distribution of intron phases - support that exon shuffling was involved in the evolution of most eukaryotic genes.
Considering how many alleles already exist in most populations of sexually reproducing animalia how on earth would you know if the occasional mutation contributed anything whatever to the processes that lead to variation, as opposed to the usual shuffling of gene frequencies among those already in existence?
-Bernd Edited by bernd, : spelling
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Faith  Suspended Member (Idle past 1465 days) Posts: 35298 From: Nevada, USA Joined: |
I cannot read links right now.
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AnswersInGenitals Member (Idle past 171 days) Posts: 673 Joined: |
Faith writes: Design difference explain all this just fine Of course. If an eye exam showed the women to have tiny Sony digital cameras in the back of her eyeball, you could honestly and accurately say 'Design difference explain all this just fine'. 'Design' can explain ANYTHING that is observed. That is why it is of such great appeal to those for whom
it's probably more time-consuming technicalities than I'm up for anyway and its why it can't be considered science.
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bernd Member (Idle past 4001 days) Posts: 95 From: Munich,Germany Joined: |
Hello Faith,
Regarding the evolution of colour vision you wrote:
I would really like to know how you think you KNOW that a mutation was involved.
Maybe we should walk step by step through the following article. The author claimes to explain “the Evolution of Trichromatic Color Vision by Opsin Gene Duplication in New World and Old World Primates”. The abstract reads:
Trichromacy in all Old World primates is dependent on separate X-linked MW and LW opsin genes that are organized into a head-to-tail tandem array flanked on the upstream side by a locus control region (LCR). The 5' regions of these two genes show homology for only the first 236 bp, although within this region, the differences are conserved in humans, chimpanzees, and two species of cercopithecoid monkeys. In contrast, most New World primates have only a single polymorphic X-linked opsin gene; all males are dichromats and trichromacy is achieved only in those females that possess a different form of this gene on each X chromosome. By sequencing the upstream region of this gene in a New World monkey, the marmoset, we have been able to demonstrate the presence of an LCR in an equivalent position to that in Old World primates. Moreover, the marmoset sequence shows extensive homology from the coding region to the LCR with the upstream sequence of the human LW gene, a distance of >3 kb, whereas homology with the human MW gene is again limited to the first 236 bp, indicating that the divergent MW sequence identifies the site of insertion of the duplicated gene. This is further supported by the presence of an incomplete Alu element on the upstream side of this insertion point in the MW gene of both humans and a cercopithecoid monkey, with additional Alu elements present further upstream. Therefore, these Alu elements may have been involved in the initial gene duplication and may also be responsible for the high frequency of gene loss and gene duplication within the opsin gene array. Full trichromacy is present in one species of New World monkey, the howler monkey, in which separate MW and LW genes are again present. In contrast to the separate genes in humans, however, the upstream sequences of the two howler genes show homology with the marmoset for at least 600 bp, which is well beyond the point of divergence of the human MW and LW genes, and each sequence is associated with a different LCR, indicating that the duplication in the howler monkey involved the entire upstream region
So far understood? If not, please pose your questions. I'll try to answer them until tomorrow. -Bernd
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