1,177 human orphan genes removed by evolutionists from databases

_{Salvador Cordova

April 13, 2014

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Here is a case of evolutionary bias causing misrecognition of orphan genes in humans. Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).

This came up in the Nelson-Velasco debate where Velasco said there are 0 orphan genes, and Nelson pointed out the reason some say they are zero is because of their biases.

Nelson has been vindicated as I pointed out in New Mechanism of Evouion — POOF

Here’s is the proof of this cover up Distinguishing protein-coding and noncoding genes in the human genome:

1. “The remaining 1,177 cases were declared to be orphans, because they lack orthology, paralogy, or homology to known genes and are not obvious artifacts… If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes… We found… 12 reported cases of orphans with experimental evidence for an encoded protein”

The problem with these authors is in 2007 they didn’t invoke the POOF mechanism of evolution which other evolutionists happily embrace now in 2013:

However, with the advent of sequencing of full genomes, it became clear that approximately 20–40% of the identified genes could not be associated with a gene family that was known before. Such genes were originally called ‘orphan’ genes

Evolutionary Origin of Orphan Genes

20-40% of the genes discovered cannot be explained by common ancestry or common descent. So what mechanism is left to explain it? Special creation? But evolutionists can’t accept special creation, so they just pretend they’ve made a discovery of a new mechanism of evolution that can work just as well.

They haven’t given it a name yet, so let us call it POOF. What is POOF? POOF is the mechanism by which proteins can easily arise out random nucleotide sequences like a poem can emerge out of randomly tossed scrabble letters. I bold one of their euphemisms for the POOF mechanism in the following paragraph:

Orphan genes may have played key roles in generating lineage specific adaptations and could be a continuous source of evolutionary novelties. Their existence suggests that functional ribonucleic acids (RNAs) and proteins can relatively easily arise out of random nucleotide sequences, although these processes still need to be experimentally explored.

😯

The reasoning they use goes like this, “we have all these genes that can’t be explained by slight successive modifications, so they must have arisen spontaneously out of nowhere. Because evolution is fact, this implies evolution can just take random material and create functional systems in a flash. We’ve made a fabulous discovery about the miracles of evolution even though we can’t demonstrate it experimentally.”

HT JoeCoder
www.reddit.com/r/creation

Comments

One way to test for non random variation is run several Lenski type experiments and see if the same point mutation emerges at a frequency higher than predicted by random change. This is too tough and expensive to do rigorously, and maybe even tougher for other kinds of mutation (indels, whatever). The amount of sequencing needed to establish non-random variation is almost unthinkable in terms of financial cost. James Shapiro cites some data that suggest some variation is non-random, but pre-programmed. That is certainly easy to believe because many protein isoforms are created in what appears a non-random way. There are MILLIONS of protein isoforms in humans that come from the 20,000 "gene" sites. If protein isoforms can be made, it is not a stretch to hypothesize "DNA isoforms", but perhaps we should be grateful the designer isn't doing too much DNA variation, otherwise it would be even harder than it is for scientists to learn about biology if the genomes were not relatively stable.scordova_{April 15, 2014
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jerry: As we have discussed here (see post #49 by Evolve, and my posts #51 and 56) there is no doubt that, at least in some cases, new protein coding gene derive from previous non coding regions. Sometimes those non coding regions have a transposon origin. However, there is at present no indication that this is the general case. Maybe it will be confirmed in many other cases, with time, or maybe not. The derivation of functional protein coding genes from non coding regions is, as I have stated many times, the best argument for design and for guided variation. As I have said in my post #59, MacNeill's list of "engines of variation" is irrelevant at best, ambiguous at worst. It puts together vague and undocumented "mechanisms", as though they could explain something. They can't. Random events are random events, whatever their form. SNPs, indels, translocations, duplications, anything that varies the genome randomly can be described as Random Variation. Classical neo darwinism is well aware of the role of RV, and MacNeill's list does not ass anything. The crucial point for the emergence of new genes remains: a) the probabilistic powers of neutral variation (extremely low) b) the algorithmic role of Natural Selection (really irrelevant) The neutral theory of evolution has shown that the role of NS is not so important as previously thought. On the other hand, neutralists tend to overemphasize the role of RV, which is irrelevant too. The simple fact is that no complex functional information can be explained out of a design theory. Other "mechanisms" invoked by MacNeill are ambiguous. They could be interpreted as algorithmic (adaptations guided by an intelligent code already existing in cells, and which incorporates actively new information from the environment), or just as forms of neo Lamarkism / epigenetics (without any detail of how they should work). Some of them are only vague appeals to undefined principles that nobody has ever shown to exist (what I call neo neo darwinism). Explanatory power: practically non existing. If we want to reason scientifically, we are always back to the same problem: it is either classical neo darwinism (driven mainly by NS) or design. And you know quite well what I think about that. :)gpuccio_{April 15, 2014
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You might want to articulate what it is you want.
I have tried and admit that I may not be as clear someone else could be who has a better grasp of the technological terms. But I am also trying to get the logic down also. I have been saying for as long as I have been commenting on this site that the debate is over the origin of new alleles. Does anyone disagree? But what does it mean to say, a new allele? I wrote a long post on it a few days ago in an attempt to make it clear what is at stake. There are two types of new alleles based on their origin and this is actually a great simplification. Anybody, please correct me I am wrong. There are those alleles that are based on coding regions already there and are just modifications of these coding regions. I believe the neutral theory only applies to these regions. Here an allele can get fixed and now the species has only brown eyes or white fur or some other characteristic that was once variable in the species but now become fixed. This is obviously a simplification since more than SNPs change. But this is not the real debate. There are alleles that arise some how de novo and I believe they could only come from non coding regions. This is what Allen MacNeill meant when he said Neo Darwinism was dead. He wasn't endorsing ID as so many thought he might by his statement. No he was advocating a much more complex naturalistic process and this is the basis of the new naturalist evolution thinking. That is why he made a big deal our of his engines of variation. I believe it over 50 now. It does kill Darwin's ideas and the modern synthesis but does not endorse anything close to ID. There are regions that do not affect the survival of the organism and thus can mutate away till someday by chance one of them turns into a region if coded can produce a functional protein. Obviously I am leaving all sorts of other areas out such as regulatory regions or epigenetic elements that control organism development or expression of a coding region. It is this latter process of allele formation which is at the heart of the naturalist process of evolution. Which is why I say the neutral theory is irrelevant. How does fixing an already existing allele account for anything meaningful in evolution? I believe there are testable hypothesis that with the current technology (the ability to map genomes quickly and expensively) that could settle the whole debate. Why, because as these non coding, non regulatory regions mutate, they will leave forensic evidence of their history. If such a thing ever existed as a true junk region turning into a functional protein then is should leave behind in those organisms which never quite reached the point where this region becomes functional a very similar sequence to the ones in those organisms that became functional. In other words if a species truly has a coding region that does not appear in a similar species then remnants of this coding region should appear in the species that does not have this coding region. It should exist as a non-coding section of DNA. And this is testable. If it doesn't exist then just how did this coding region arise? They must have existed before a sub-population split off and thus could not inner breed. It takes millions of years to form these de novo coding regions so they should be evident in the other populations before the split happened. Personally, I think this is mathematically impossible but for de novo coding regions to arise it must have happened in this way and if it did it would leave a trail of dead ends in similar species.jerry_{April 15, 2014
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Moran is wrong- junk DNA is not evidence against NS. You would think it would but seeing that it is neither fatal nor detrimental, it doesn't get eliminated. That said, NS is still their only alleged "designer mimic". It just makes the most of the relatively few opportunities.Joe_{April 15, 2014
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I am under the impression that the neutral theory which has received a large number of posts and comments here lately is essentially a side issue in the evolution debate and that the origin of new genes/alleles and their corresponding coding of new proteins is where the real debate lies.
Neutral theory is important because it is the one case where the mainstream agrees with IDists and creationists -- Natural Selection as a matter of principle has little role in molecular evolution, either origination or maintenance of design. Moran says, "well evidence of selection's absence is all the junk in the genome", IDists say "the genome isn't junk, and neutral theory says all that intricacy can't be by selection, so it's by design."
It would be very helpful if one of the authors made a detailed OP on the different issues with genes, coding regions, orphan genes, expressed proteins, origins of the coding regions, etc.
Gpuccio seems to be the man for the job. :-) But that's a lot for just one post. How about breaking it down to several posts. You might want to articulate what it is you want.scordova_{April 15, 2014
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Evolve- Please model blind and unguided processes producing protein coding genes from non-coding DNA. Or admit that the claim is unscientific. Thank you.Joe_{April 15, 2014
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I will see if I can find the reference.
Allen MacNeill recommended a book edited by Elisabeth Vrba and Niles Eldredge titled "Macroevolution: Diversity, Disparity, Contingency" The first article is titled "Disparity, Adaptation, Exaptation, Bookkeeping, and Contingency at the Genome Level" by Jürgen Brosius. In this article he lays out the basic process that create novel coding areas for new proteins. It is all assertion with no proof but it points to what they are hanging their hat on. It is not the neutral theory. An aside: Brosius is a low life.jerry_{April 14, 2014
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Please ignore that last post from me. I have no idea how that happened but somehow extra text that I did not type was inserted.Jehu_{April 14, 2014
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Jerry, Funny that the post immediately following the one you linked to was from me. Okay, so you get it. It can be extrapolated from Behe's well supported arguments that all this talk about neutral drift is a non-starter for Darwinist evolution and orphan genes are further damning evidence against the theory. In Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes.~10^20 reproductive events you get two mutational steps. That is it. One neutral, one selected. Darwinism does not have enough creative power in all of geological time to create most these genes.Jehu_{April 14, 2014
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jerry at #55:
It is not the neutral theory but mutations of non coding regions that is at the heart of the argument. I will see if I can find the reference. It was something Allen MacNeill advised us to read about 6 years ago. It was in a special issue of a journal on Stephen Gould. That is why Allen pushed real hard on his engines of variation. This all goes back about 6 years ago.
The problem, with MacNeill's "engines of variation", is simply that either they are guided (and therefore they are tools of design) or they are random, and therefore add nothing to random mutations. RV is the sum of SNP + any other kind of random variation. A few of those mechanisms could be algorithmic, IOWs adaptive. In that case, they are certainly very complex, and they must be considered as designed algorithms. In the end, design is the only good explanation for what we observe.gpuccio_{April 14, 2014
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Thanks for the explanations and links, gpuccio. I wasn't aware of the three human-specific genes that you mentioned.
As you can see, even if the neodarwinist bias is constantly trying to obfuscate biological research, there are always good scientists who do their good work.
Or, more generously, the neodarwinist paradigm (or idealogical contamination in some cases) has undeniably slowed scientific progress as a result. -QQuerius_{April 14, 2014
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Ok, great! As you know, Behe doesn't rule out other, unnamed mechanisms. He just points out the limitations of mutation. So, instead of looking for other mechanisms, evolutionists simply attacked Behe. Much easier than doing science. -QQuerius_{April 14, 2014
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Querius at #52: Yes. That's an important point. Even genes that are supposed to evolve by neutral mutations only, like would be the case for genes which derive from non functional sequences (non coding DNA or inactivated gene duplicatins) would require NS at the end of the process, to be expanded and fixed in the population, otherwise they would soon be lost, and all the impossible result against all the probabilistic laws would be for nothing! :) That is a further problem for the impossible model of neutral evolution of function, because in some way it would be necessary that the "evolved" sequence, which by definition has no reason to be translated, not being an ORF, should become translated (in the right quantity, in the right context) as soon as it is "ready". Otherwise, living cells would be repleted of non functional proteins which are being translated in the long time in which they evolve, so that they may be continuously tested by NS, which is not exactly supported by facts. See also my posts #58, 72 and 73 in VJ's thread. "When I am wrong", here: https://uncommondescent.com/intelligent-design/when-im-wrong/ I would like to add, to the papers suggested by Evolve, this important paper about humans: http://genome.cshlp.org/content/19/10/1752.full.pdf The abstract:
The origin of new genes is extremely important to evolutionary innovation. Most new genes arise from existing genes through duplication or recombination. The origin of new genes from noncoding DNA is extremely rare, and very few eukaryotic examples are known. We present evidence for the de novo origin of at least three human protein-coding genes since the divergence with chimp. Each of these genes has no protein-coding homologs in any other genome, but is supported by evidence from expression and, importantly, proteomics data. The absence of these genes in chimp and macaque cannot be explained by sequencing gaps or annotation error. High-quality sequence data indicate that these loci are noncoding DNA in other primates. Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages. The genes are not well characterized, but interestingly, one of them was first identified as an up-regulated gene in chronic lymphocytic leukemia. This is the first evidence for entirely novel human-specific protein-coding genes originating from ancestrally noncoding sequences. We estimate that 0.075% of human genes may have originated through this mechanism leading to a total expectation of 18 such cases in a genome of 24,000 protein-coding genes.
And look at this important statement in the discussion:
We hypothesize that there are at least two steps in the evolution of a novel protein-coding gene from ancestrally noncoding DNA. The DNA must become transcribed and it must also gain a translatable ORF. These steps may occur in either order so that a transcribed locus that does not originally encode a protein, perhaps even an RNA gene, may acquire an ORF. Alternatively, a new ORF, once created by mutation, may become transcribed, for example, through the serendipitous use of a nearby existing gene promoter. Here we have documented particular DNA sequence changes in the evolution of three human-specific ORFs and have demonstrated in each case that at least one critical mutation that enables the ORF is human-specific because an identical disabled state is found in chimp, gorilla, gibbon, and macaque. We cannot, at present, determine whether the ORF originated before or after expression was acquired because EST coverage is so low for chimp. However, such an analysis would not be informative in any case because we are sure that chimp cannot produce any of these proteins; so, irrespective of RNA expression, the protein-coding gene can only be present in human.
And, finally:
The three genes reported here are the first well-supported cases of protein-coding genes that arose in the human lineage and are not found in any other organism. It is tempting to infer that human-specific genes are at least partly responsible for human-specific traits and it will be very interesting to investigate the functions of these novel genes.
As you can see, even if the neodarwinist bias is constantly trying to obfuscate biological research, there are always good scientists who do their good work. :)gpuccio_{April 14, 2014
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I recommend Behe’s Edge of Evolution as a background primer in how genes may or may not evolve. Most posters here are familiar with the arguments made therein. Read the actual book as most of the reviews flat out lie about the contents.
I was the probably the first one on this site to have read the book and commented on it. I knew instantly the implications of the book. https://uncommondescent.com/intelligent-design/so-many-id-books-so-little-time-id-sympathetic-book-by-gingerich-2006/#comment-125290 https://uncommondescent.com/intelligent-design/so-many-id-books-so-little-time-id-sympathetic-book-by-gingerich-2006/#comment-125324
My comments are not based on being behind but seeing that what is being discussed is irrelevant from what I have read in the past. So far no one has told me why the neutral theory isn't irrelevant?
I was also one of the first ones on this site to have read the basis of evolution from the naturalist point of view. It is not the neutral theory but mutations of non coding regions that is at the heart of the argument. I will see if I can find the reference. It was something Allen MacNeill advised us to read about 6 years ago. It was in a special issue of a journal on Stephen Gould. That is why Allen pushed real hard on his engines of variation. This all goes back about 6 years ago.jerry_{April 14, 2014
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Jerry, I'd like to second Jehu's recommendation. Please realize that Behe is NOT an anti-evolutionist, but the limits of one of the basic mechanisms of evolution is what he examines based on his research on malaria. -QQuerius_{April 14, 2014
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Jerry, I recommend Behe's Edge of Evolution as a background primer in how genes may or may not evolve. Most posters here are familiar with the arguments made therein. Read the actual book as most of the reviews flat out lie about the contents.Jehu_{April 14, 2014
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gpuccio, Wouldn't NS affect the results of newly expressed functional genes? -QQuerius_{April 14, 2014
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Evolve: I absolutely agree with you that new genes can arise and do arise from non coding DNA, and I have already stated that in answer to a previous post of yours. That is a very strong argument for design. The origin of new functional genes from non coding DNA cancels completely the role of NS. So, it is a very strong argument for design. I don't think, however, that there is any evidence that all, or most, of the new genes arise from non coding DNA. In the case of human orphan genes, I have found no evidence for that in the quoted articles.gpuccio_{April 14, 2014
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Having lost all arguments, creationists are now trying to hold on to their last strand of hope
This is an absurd statement. Maybe there should be a new logical fallacy,
"arguing from the absurd."
Besides, what is meant by the term, "creationist?"jerry_{April 14, 2014
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Having lost all arguments, creationists are now trying to hold on to their last strand of hope - ORFans. Almost every other post by Vincent Torley and Sal Cordova mentions them! But there's no hope for creationists here too. I had, in fact, pointed out in one of Vincent Torley's threads a few new studies showing how de Novo gene synthesis happens from non-coding DNA. Curiously he seems to have ignored all the evidence and keeps on repeating science has no idea how ORFans arise. I'm re-posting papers reporting origin of new genes from intergenic DNA: 1. Emergence of a New Gene from an Intergenic Region (in Mouse) http://www.sciencedirect.com/science/article/pii/S0960982209014754 2. Origin and Spread of de Novo Genes in Drosophila melanogaster Populations http://www.sciencemag.org/content/343/6172/769.abstract 3. Female fly genomes also populated with de novo genes derived from ancestral sequences http://phys.org/news/2014-03-female-genomes-populated-de-novo.html It's clear as broad daylight that ORFans can arise by mutations in intergenic DNA. Sal Cordova & Vincent Torley can continue to express amazement at how that's possible!Evolve_{April 14, 2014
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In my previous post above I am questioning the usefulness of the neutral theory of evolution as having any meaningful effect on evolution. In one of Dr. Torley's posts, there was a map of human migration across the globe https://uncommondescent.com/intelligent-design/branko-kozulic-responds-to-professor-moran/ In it one of the most isolated populations on the planet were the inhabitants of Australia which first went there 50,000 years ago. That represents about 1800-2000 generations. So we have the perfect natural experiment. There must be a lot of different fixed mutations in this population than are in say, African or Western European genomes. So someone should do the research and settle the question.jerry_{April 14, 2014
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It would be very helpful if one of the authors made a detailed OP on the different issues with genes, coding regions, orphan genes, expressed proteins, origins of the coding regions, etc. I am under the impression that the neutral theory which has received a large number of posts and comments here lately is essentially a side issue in the evolution debate and that the origin of new genes/alleles and their corresponding coding of new proteins is where the real debate lies. So a lot of meaningless comments get made on issues which are either not very relevant or which no ones knows much about. Thus, an OP on this might eliminate a lot of the fog which surrounds these and related topics. And as an addendum to this, a discussion on those regions that seem to be conserved across species and over time within a species would be appropriate since conserved regions means that these regions are selected for and thus preserved and thus have a necessary function. Otherwise the famous engines of mutation would drive them apart within any population and and most certainly across species. Would be enlightening and eliminate a lot of wasted pixels.jerry_{April 14, 2014
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Gpuccio, perhaps several thousand genes could be ORFans given the >39% of orphan enzymatic activities of humans. (Or else alternative splicing is far more radical than previously envisioned) Orphan enzymes could be an unexplored reservoir of new drug targets. - 2006 Excerpt: Despite the immense progress of genomics, and the current availability of several hundreds of thousands of amino acid sequences, >39% of well-defined enzyme activities (as represented by enzyme commission, EC, numbers) are not associated with any sequence. http://www.ncbi.nlm.nih.gov/pubmed/16580971bornagain77_{April 14, 2014
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Gpuccio I completely agree with you and your previous posts on the matter. I was also just trying to bring a practical example to the table as I think it is useful to see this us a day-to-day observation in practical science as opposed to something just spoken of in a paper and published (very often the two do not converge as we would hope or expect!). Thanks, JDDr JDD_{April 14, 2014
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BA: Thank you for linking to that old post of mine. I think it remains valid. They simply want to interpret those ORFs as arising from coding gene regions, instead of just thinking that they could be coding genes. Pure bias.gpuccio_{April 14, 2014
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Dr JDD: I absolutely agree with you, and I have erxpressed similar ideas in posts 25 and 30. I would add that, in this particular case, given the huge phenotypical differences between humans and chimps, and the minor differences in known protein coding genes, which can scarcely begin to explain those differences, it should be the primary duty of researchers to concentrate on DNA differences between the two species. 1177 potentially protein coding sequences which are completely new should really be at the center of attention, not to deny their importance, but rather to verify their functional meaning. Even if they were not protein coding genes, they could just the same be regulatory genes. However, they should be thoroughly investigated. Instead, what do we see? Academic scientists do their best to simply deny their importance and to delete them from the ORF database. And how do they do that? Simply showing that, if they were really protein coding genes, their personal model (neo darwinism) could not explain them. For me, this is cognitive bias at its worst.gpuccio_{April 14, 2014
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Dr. JDD, Actually authors of the preceding 'kick the ORFans out in the street' paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias: https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/comment-page-6/#comment-358547bornagain77_{April 14, 2014
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RE #6 (Moose D=r) –I would personally have to somewhat disagree with this:
I don’t see them shutting down inquiry. They seem to want to keep orphans out of the gene databases until a protein is verified. This position should spur exploration into the 1177 to find produced proteins. At least hopefully.
The reason I disagree is from a practical experience point. When I have done risk analyses by BLAST searching the human genome for short peptides of a specific length (to assess risk of a protein we have made to detect this peptide), we often come across many proteins that when you try to design primers and find tissues where it is expressed, you have trouble. When you trace it back and look at the data it is most likely an ORF that is a predicted protein. There are 100s of these in the human databases that we use, that have no “evidence of protein” available yet in the literature, yet they are still included on the hit list (and not relegated further down the list of priority, just because there is no evidence of actual protein translated from this sequence). Therefore despite me not being a geneticist and rather a cell biologist, I would conclude that there are in fact many ORFs with no evidence of protein from these yet they are included in databases that most scientists use. As such, I cannot agree that there practically is a drive to “keep orphans out of the gene databases until a protein is verified” as this is not what I personally experience on a day to day basis. Although I can admit, I may be wrong in that there is some other evidence besides what is listed there (protein evidence or lack of) for its inclusion in these databases, but this is not how it appears, and to quote my colleagues in the relevant department when I ask if this is a real risk, "This probably is a gene that does not exist as a protein" (therefore they take it as a hypothetical ORF that is present in the database). We would be good to remember though that as pointed out here, lack of evidence at this stage could be due to lack of understanding the right conditions and mechanism for expression of said ORF into a real protein (much like the junk DNA theory commonly subscribed to 10 years ago). JDDr JDD_{April 14, 2014
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Are you a Christian Sal? At times I really wonder.Mung_{April 14, 2014
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Salvador:
Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).
No, Sal, that's not what an orphan gene is. Here's the link to the Wikipedia article. Here's how the Discovery Institute defines them:
orphan genes (protein-coding sequences without known protein-coding antecedents)
And there's this:
Orphan genes are protein-coding regions that have no recognizable homolog in distantly related species.
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?Mung_{April 14, 2014
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