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Is the vitamin C-making pseudogene evidence of shared ancestry?

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On 12/1/2017 at 12:27 AM, Tristen said:

A very large percentage have no observable function at all.

'Not observed' is a different claim to not “observable”. The latter is not a justifiable claim until you have investigated every possible “temporo-spatial” circumstance that the gene might be designed to respond to.

You are right, I should have been more careful in my language. I should have used "observed" rather than "observable".

On 12/1/2017 at 12:27 AM, Tristen said:

The problem is that you have constructed an argument that relies on the non-functionality of pseudogenes. Your argument is that common mutation patterns found in non-functional genes indicates shared ancestry. But if a described pseudogene has a function, then it is simply a gene that resembles another gene. Similarities in (functional) genes between species is an entirely different discussion to the one we are having. But the argument in your OP is given weight by the assumption that the genes are non-functional, and therefore, unlike functional genes, have no reason to share similar changes (from the original gene) across species, apart from mutation patterns inherited through shared ancestry.

I would phrase my argument slightly differently. You are correct that function has been determined for a small percentage of pseudogenes. So I would argue that pseudogenes have lost the same function as the original counterpart genes. I think we can both agree that this is true for a great majority of the pseudogenes. It is the specific class of pseudogenes (the unitary pseudogenes, including GULOP) that I believe makes a strong argument for common ancestry. Whereas most pseudogenes have a counterpart in the same genome, the unitary pseudogenes do not. To find a homolog of the GULOP that encodes an enzyme for vitamin C synthesis, we have to look to other vertebrates. The group of primates that are most-closely associated with humans due to DNA similarity also show the same loss of vitamin C synthesis because the pseudogene in those primates also lacks the same exons. Here is a reference (https://link.springer.com/article/10.1007%2Fs10528-013-9574-0) that is behind a paywall. I'm working on obtaining a PDF, but you may be able to access it.

On 12/1/2017 at 12:27 AM, Tristen said:

The conclusion is a plausible (and most plausible, in my opinion) explanation of observed fact.

Your “opinion” that your preferred “conclusion” is the “most plausible” in no way obligates someone with a contrary opinion to accept either your assumptions, opinions or conclusions.

Oh, you are absolutely correct! I would be rather aghast if you took my explanation as sufficient for you to change your entire viewpoint. 

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1 hour ago, Saved.One.by.Grace said:

Are you attempting to use this observation between pseudogenes and functionality common between mammals and humans as a basis for support for evolutionary theory?  Do we know that all mammals and all humans have lost the ability to synthesize vitamin C or only those tested experimentally?  Could it be we do not fully understand God's programming language, DNA, and what it does with respect to its host?

I'm suggesting that the similarities in exon loss in the GULO pseudogene that exist between humans and what scientists consider closely-related primates is evidence of common ancestry. Humans are incapable of producing vitamin C, as are gorillas and chimps, which scientists consider our closest neighbors, according to DNA sequence similarities.

It would seem rather coincidental that humans and related primates all lack the ability to make vitamin C, while more distantly-related primates and many other mammals have retained this ability. The observed coincidence is even stronger when the reason for that lost ability becomes evident. We all have GULO pseudogenes that have lost the exact same exons (protein-encoding portions of genes).

image.png

This figure is from a paper (https://link.springer.com/article/10.1007/s10528-013-9574-0) published in 2013. Although the figure only lists human, chimpanzee, and macaque, it should be noted that gorilla and orangutan sequences also are missing the same exons. Additionally, for the exons that are shared between these species, the sequence identity ranges between 75-99%. All in all, I feel that the GULO pseudogene is a rather strong piece of evidence supporting common ancestry.

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41 minutes ago, Saved.One.by.Grace said:

This, of course, violates the 2nd Law of Thermodynamics.

Actually, the constant energy input from the sun allows increased organization without violation of the 2nd law of thermodynamics.

43 minutes ago, Saved.One.by.Grace said:

All living organisms breakdown to simpler life forms before death.

Would you say you were more complex as a single-celled zygote, or as an adult, composed of trillions of coordinated cells?

44 minutes ago, Saved.One.by.Grace said:

I believe God is the programmer.

Me, too.

44 minutes ago, Saved.One.by.Grace said:

It makes sense for God to be consistent in His programming only varying what needs to be varied.

This point can be made for functional genes, but recall that the GULO pseudogene is (or certainly appears to be!) a mutated and broken version of a functional gene involved in vitamin C synthesis. Why would God put the same nonfunctional version of a gene in apes and ape-like primates?

 

59 minutes ago, Saved.One.by.Grace said:

We share 50% of our DNA with bananas.  We share 99.9% of our DNA with the person sitting next to you, and 98.8 +/- .2% with Chimps.  Is it cannibalism to eat bananas?  We are also related to cats and cows.  It is awesome what God can do with a slight change in the code that makes you, well you.

The figures for humans and chimps is accurate, depending on exactly what is being compared in the chimps. But this tends to support common ancestry, not invalidate it. The figure for bananas is widely spread throughout the internet, but is far from accurate. Out of all the protein-coding genes in the human genome, it is conceivable that about 50% may share some DNA similarity (~25% or greater) to genes in bananas. But when we realize that genes make up less than 5% of the human genome, and the remaining 95+% is completely unrelated to the banana, you can see why that figure is inaccurate. In other words, the tremendously high similarity between chimps and humans is pretty convincing evidence of shared ancestry to a vast majority of scientists.

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On 05/12/2017 at 1:15 AM, one.opinion said:

You are right, I should have been more careful in my language. I should have used "observed" rather than "observable".

I would phrase my argument slightly differently. You are correct that function has been determined for a small percentage of pseudogenes. So I would argue that pseudogenes have lost the same function as the original counterpart genes. I think we can both agree that this is true for a great majority of the pseudogenes. It is the specific class of pseudogenes (the unitary pseudogenes, including GULOP) that I believe makes a strong argument for common ancestry. Whereas most pseudogenes have a counterpart in the same genome, the unitary pseudogenes do not. To find a homolog of the GULOP that encodes an enzyme for vitamin C synthesis, we have to look to other vertebrates. The group of primates that are most-closely associated with humans due to DNA similarity also show the same loss of vitamin C synthesis because the pseudogene in those primates also lacks the same exons. Here is a reference (https://link.springer.com/article/10.1007%2Fs10528-013-9574-0) that is behind a paywall. I'm working on obtaining a PDF, but you may be able to access it.

Oh, you are absolutely correct! I would be rather aghast if you took my explanation as sufficient for you to change your entire viewpoint. 

Hey One,

You are correct that function has been determined for a small percentage of pseudogenes. So I would argue that pseudogenes have lost the same function as the original counterpart genes.”

If a gene has a function, then it is a gene (i.e. “pseudogene” is a misnomer). You may “argue” that it is derived from a mutated version of another gene, but that is an unverifiable claim about the history of the gene. A functional gene is a functional gene, and could just as readily be considered a gene in its own right.

 

I think we can both agree that this is true for a great majority of the pseudogenes.”

I don’t think I would be comfortable with that generalisation; especially not for those genes with known functions. I have no problem with the existence of mutations changing genes, but to assume that for any specific example requires assuming the history of the gene (unless the change has been observed over generations).

 

It is the specific class of pseudogenes (the unitary pseudogenes, including GULOP) that I believe makes a strong argument for common ancestry. Whereas most pseudogenes have a counterpart in the same genome, the unitary pseudogenes do not. To find a homolog of the GULOP that encodes an enzyme for vitamin C synthesis, we have to look to other vertebrates. The group of primates that are most-closely associated with humans due to DNA similarity also show the same loss of vitamin C synthesis because the pseudogene in those primates also lacks the same exons. Here is a reference (https://link.springer.com/article/10.1007%2Fs10528-013-9574-0) that is behind a paywall. I'm working on obtaining a PDF, but you may be able to access it.

I got the paper.

It is unfortunate that most of the relevant sequence information for the primates was missing. And it’s nice how they inserted the “lost” exons in their picture of the human genome (albeit dark grey instead of black) to show where the exons supposedly ‘used to be’ – and so graphically reinforcing their impression of evolutionary history. But for the sake of argument, let’s accept the proposition that these primates share 6 of the 11 GULO exons (12 exons according to figure 1 in this article) present in most other vertebrates.

Yang (the author) generally uses well-hedged language, except when talking about secular evolution. The a-priori acceptance of this premise is clear in the nature of the language used.

During vertebrate evolution, some species, including anthropoid primates (Nishikimi et al. 1994), guinea pigs (Nishikimi et al. 1992), teleost fishes (Dabrowski 1990), some bats (Cui et al. 2011), and certain passerine birds (Chaudhuri and Chatterjee 1969), lost their ability to synthesize vitamin C, mainly through the loss of their GULO genes.

Note that this is expressed as fact, even though it is not fact. The facts are that certain primates cannot synthesise vitamin C, and that these primates share some exons with the gene that synthesises vitamin C in other species. How those facts came to exist is historical speculation.

Note how this presupposition dictates the historical assertion that these exons were “lost”;

Among the 15 GULO-less animals, some (such as teleost fishes) have really lost their GULO genes

And in their figure 1,

exons that have accumulated too many mutations to be recognized (dark gray marked ‘‘Lost’’)

So we return to a mutation-of-the-gaps argument.

Higher primates, including the human, orangutan, chimpanzee, gibbon, and macaque, have lost nearly half of the 11 exons.”

Among the vertebrate species that cannot produce AsA, teleost fishes and higher primates both lost their GULO genes in remote ancestors; most bats and guinea pigs also lost their GULO genes during evolution.”

And just in case you missed it,

Vertebrate GULO genes are conserved except for those that are lost.” (I think there’s something in that for all of us).

I hope you understand by now that asserting they were “lost” assumes they were there to begin with. That is not established by the facts.

The facts are as follows (given we assume the missing information concurs); A certain group of primates have sequences containing 6 of the 12 exons found in functioning GULO. Now we might get the impression they are similar (from the way they’re lined up in figure 1), but in reality, 6 less exons represents a massive structural difference. “Nearly half of the 11 exons” are missing in these “Higher primates”. In no sense is that a trivial difference.

How can we even assume they are the same gene? There are several known genes with different functions that contain the same exons as other genes. This paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4450672/) describes the LDL gene having 18 exons; “Thirteen of the 18 exons encode protein sequences that are homologous to sequences in other proteins: five of these exons encode a sequence similar to one in the C9 component of complement; three exons encode a sequence similar to a repeat sequence in the precursor for epidermal growth factor (EGF) and in three proteins of the blood clotting system (factor IX, factor X, and protein C); and five other exons encode nonrepeated sequences that are shared only with the EGF precursor.” Of course appropriate homage is paid to the secular evolution story; “One likely mechanism for such sharing is through the duplication and migration of exons during evolution”. This other paper (https://www.sciencedirect.com/science/article/pii/S0888754399961128), shows 7 exon homologs appearing in two genes. So we cannot assume GULO and GULOP are the same gene simply based on shared homology between some exons.

Even if they were identical genes (exon-wise), we could not assume that the gene is limited to a single function. Yang (http://www.cell.com/cell/fulltext/S0092-8674(16)30043-5 ) (a different Yang to the paper you provided) demonstrated clearly that a single gene can have many functions due to alternate splicing. That is, “the existence of introns permits functional domains encoded by discrete exons to shuffle between different proteins” (quoting Sudhof – from the sciencedirect reference above). Everyone is assuming that GULO only does one thing (synthesises vitamin C). But that can’t be determined without extensive analysis. Why does GULO need 12 exons to perform a single function? How do we know there’s not a function for the 6 exons in the primate GULOP? Until we’ve investigated all the potential isoforms and “proteoforms”, we can’t justify that assumption. Yang (my Yang, not your Yang) investigated roughly 1500 human genes from 16 kinds of tissue. They unfortunately didn’t look into GULOP – probably because it has been designated a pseudogene with an already assigned ‘evolutionary’ history and non-functionality. That is the problem when assuming no known function equals no function – who wants to investigate a gene that everyone ‘already knows’ is useless?

Even if GULOP is now a true pseudogene (i.e. a broken version of another gene), that doesn’t mean vitamin C synthesis is the only possible function the original gene performed.

Regardless of which paradigm you prefer, the primates with GULOP have never needed to synthesise their own vitamin C. This function has never been necessary in these creatures. Whether the 6-or-so thousand years I propose, or the “about 63 million years ago” proposed by Yang (your Yang), the reality is, we have all survived just fine without the need to synthesise our own vitamin C. The only paradigm requiring vitamin C synthesis in our ancestry is the one that assumes we ‘evolved’ from lessor forms which may not have had Vitamin C in their diets.

Your Yang even repeats the story of how some bat species “regained active GULO”. “These repeated losses and gains of the GULO gene were also observed in some passerine birds”. The idea of permanent inactivation doesn’t suit other aspects of the evolution story. Must have been mutations reactivating the genes. Wondrous things mutations. What can’t they do?

 

So let’s consider the story you are proposing. Between 61 and 63 million years ago (i.e. after the separation of Haplorhini from the sister primate order Strepsirhini, but before the Haplorhini speciated into the diverse range of higher primates we see today), there was a massive mutation event which selectively deleted 6 exons from the GULO gene. But not the first 6, or last 6, or 6 in the middle – this event completely annihilated exons 1, 2, 3, 6, 8, & 11, whilst skipping over the other 6 interspersed exons – leaving them untouched. And the remaining exons have miraculously been conserved over that 60-or-so million years of evolution, despite the accumulation of evolutionary differences between the higher primates, and despite having no selective advantage in the maintenance of such a large, useless gene.

Since we are offering opinions, I think that story defies credulity. I think GULOP in higher primates is sufficiently different from GULO to argue that it was never GULO, but more likely a different gene (or a pseudogene with an origin different to GULO). That would place it into the argument category of ‘similar creatures designed to fulfill similar niches in similar environments have similar information incorporated into their genomes’.

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1 hour ago, Tristen said:

So let’s consider the story you are proposing. Between 61 and 63 million years ago (i.e. after the separation of Haplorhini from the sister primate order Strepsirhini, but before the Haplorhini speciated into the diverse range of higher primates we see today), there was a massive mutation event which selectively deleted 6 exons from the GULO gene. But not the first 6, or last 6, or 6 in the middle – this event completely annihilated exons 1, 2, 3, 6, 8, & 11, whilst skipping over the other 6 interspersed exons – leaving them untouched. And the remaining exons have miraculously been conserved over that 60-or-so million years of evolution, despite the accumulation of evolutionary differences between the higher primates, and despite having no selective advantage in the maintenance of such a large, useless gene.

To be completely fair, no one is claiming there was a single event that selectively removed 6 different non-sequential exons. The claim is that the exons were lost (in one way or another) prior to a divergence point leading to the existing anthropoid primates.

I do admit that the high degree of homology in the existing exons is indeed perplexing, especially if it truly has lost function. However, to date that there is exactly zero current evidence of the GULOP sequence performing any other type of function. I would have to check some sources again, but I don't think the GULOP is even transcribed. But it would be interesting to see research into possible functions.

 

 

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1 hour ago, Saved.One.by.Grace said:

Why is 90% of our DNA match for a house cat?

Just like with the banana, there is a vast difference between the following statements:

1.  Human DNA is a 90% match to cat DNA.

2.  90% of human genes have some homology with cat genes.

The first statement ignores the 95+% of the genome that is not protein-coding. I don't know what the overall sequence similarity is, but it is nowhere near 90%.

1 hour ago, Saved.One.by.Grace said:
2 hours ago, one.opinion said:

Actually, the constant energy input from the sun allows increased organization without violation of the 2nd law of thermodynamics.

False.  Prove it.

Life proves it. Repeatedly. Every time a multicellular organism grows from a zygote.

1 hour ago, Saved.One.by.Grace said:

But I want to be extra serious for a moment.

There is systematic plan to devalue human life.  The Theory of Evolution is part of it, The Holocaust too, so is Abortion and Planned Parenthood.  A lot of people, maybe most people will scoff at that.  But there's a reason for humans devaluing themselves.  We will think less of ourselves if there is less difference between us and the animals.  There is an organized effort to separate us from the perfect will of our savior Jesus, how Jesus sees us and values us enough to give His life to rescue ours. 

I agree that there is a trend toward devaluing life. I will disagree with the role of the theory of evolution, though. The theory is only an explanation (whether one agrees or disagrees) with observed facts. It doesn't say anything about the value of life. The theory of evolution has been repeatedly and tragically applied in very horrific ways, but it is not responsible. That is like blaming cheeseburgers for my expanding waistline. The existence of the cheeseburger doesn't make me fat, it is my misuse (in this case, overindulgence) that makes me fat.

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3 hours ago, one.opinion said:

Actually, the constant energy input from the sun allows increased organization without violation of the 2nd law of thermodynamics.

Clumsily False...

In Biologic Systems, to build "Functional Sequence/Specified Complexity" (Cellular Structures) you need a SPECIFIC Energy Converter (i.e., Mitochondria/Chloroplasts/Metabolic Pathways) and INFORMATION Program (DNA) ALREADY EXISTING FIRST so as to capture, convert, and use the energy meaningfully.  
Extracellular Nucleo-Bases and Amino's are DESTROYED by Sunlight as is virtually everything on the planet without the Energy Converter/Information Program already existing. The Sun's energy without the aforementioned conditions existing FIRST is like a Bull in a China Shop.

Real World Example: Mid Summer in Texas, the Sun is destructive.  It will burn the tires clean off a tractor if left in the field long enough. And it will eventually do the same with the roof on your house and your car if not protected.  Why?  Because there is no "Pre-Existing" mechanism to capture the heat of the sun and an information program to direct its use.  Now let's put solar panels on the roof, and add an information program (computer/software) to capture the sun's energy and direct it to produce electricity.  Now the sun is no longer destructive.  But--and this is important, the sun will NEVER build the solar panels or write a program to convert the heat to usable energy. 

See the "Specific" Energy Converter and Information Program in the above example?

Or do you ascribe to the Sun sending Intelligent Messages or Instructions to "Stupid" Atoms so they can build it?

 

Quote

In other words, the tremendously high similarity between chimps and humans is pretty convincing evidence of shared ancestry to a vast majority of scientists.

Clumsily False:

1.  If ancestry is not assumed from similarities, then there is no correlation between similarities and ancestry; Ergo, to make the argument you need to make that "assumption". i.e., Begging The Question Fallacy.
 
All you have is a TEXTBOOK...Affirming The Consequent (Formal Logical Fallacy):

If P then Q.
Q.
Therefore P.

1. IF evolution is true "P": then Insert any "Darwinian Grab-Bag" Post-Hoc Observations (Fossils/Homology/Similarity/Genetic Variation et al) "Q".
2. We observe (Post Hoc Observation) "Q".
3. Therefore, Evolution is true. "Therefore P".

Or...

If Common Descent is True "P" we will observe Genetic Similarities "Q".
We Observe Genetic Similarities "Q".
Therefore, Common Descent is True. "Therefore P".


The logical fallacy is that "P" doesn't necessarily follow from "Q"

e.g.,
 
1)  If I had just eaten a whole pizza "P", I would feel very full "Q" ;
2)  I feel very full "Q";
3.) Therefore: I have just eaten a whole pizza. "Therefore P".
 
Couldn't I have eaten a 20 ounce Ribeye with Fries or the ole 96'er (!!!) ?


Let's put this quackery out of it's Misery QUICK!!! ...

Dr. Craig Venter; The Grand Poobah of Geneticists, The Geneticists of Geneticists... 

"There is NO TREE OF LIFE ...it's an artifact from early scientific studies that aren't holding up...

"So THERE IS NOT A TREE OF LIFE."
Craig Venter PhD Geneticist (NIH, Celera Genomics); Arizona State Origins Project; 12 February 2011 (TIME: 9:14)

The Audience Gasped, Dawkins and Krauss turned different shades of GREEN.
Ya hear that sound?? ...that's the "Common Descent" Fairytale TREE circling the drain @ Light Speed !!! ("as if" he actually needed to say it).

 

2.  “For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee."
Ebersberger, I. et al: Mapping human genetic ancestry, Molecular Biology and Evolution, Vol. 24(10):2266-2276 (2007)
 
Down to 77% right quick!!  That ='s 690 Million Base Pairs, roughly 227 Large Books!

And, Bear in mind....Even if humans were ‘only’ 4% different this still amounts to 120 million base pairs, equivalent to approximately 12 million words, or 40 large books of information. 

 

Quote

...pretty convincing evidence of shared ancestry to a vast majority of scientists.

1.  They're NOT "Scientists".

2.  Appeal to Consensus/Majority (Fallacy).

3.  This isn't Scientific Evidence (See Above)...it's a Logical Trainwreck of Epic Proportions.  To refute, Scientifically Validate "Shared Ancestry"...

a.  What Phenomenon was Observed...?
b.  Post the Formal Scientific Hypothesis then EXPERIMENT that validates your claim...?
c.  Highlight the "Independent Variable" that was used in the TEST...?
d.  Post the Null Hypothesis that was Rejected/Falsified...?

 

regards

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19 minutes ago, one.opinion said:

I will disagree with the role of the theory of evolution, though. The theory is only an explanation (whether one agrees or disagrees) with observed facts.

 

For the 2678th Time:  'evolution'?? :huh: What's  that...?  Define evolution...?  

a.  Post the Scientific Theory of evolution...? 
b.  Post just TWO Formal Scientific Hypotheses then Experiments that concretized it into a *REAL* Scientific Theory...?
c.  Post the Null Hypotheses that were Rejected/Falsified for each...?
d.  Highlight The Independent Variables used in Each TEST...?

 

Quote

It doesn't say anything about the value of life.

It doesn't say anything! 

1.  It doesn't and NEVER Existed.

2. Even if it did exist, it wouldn't have Vocal Chords; Ergo...Reification Fallacy.

 

regards

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54 minutes ago, one.opinion said:

To be completely fair, no one is claiming there was a single event that selectively removed 6 different non-sequential exons. The claim is that the exons were lost (in one way or another) prior to a divergence point leading to the existing anthropoid primates.

I do admit that the high degree of homology in the existing exons is indeed perplexing, especially if it truly has lost function. However, to date that there is exactly zero current evidence of the GULOP sequence performing any other type of function. I would have to check some sources again, but I don't think the GULOP is even transcribed. But it would be interesting to see research into possible functions.

" To be completely fair, no one is claiming there was a single event that selectively removed 6 different non-sequential exons. The claim is that the exons were lost (in one way or another) prior to a divergence point leading to the existing anthropoid primates. "

Not just "prior to a divergence point leading to the existing anthropoid primates", but also after the separation of Haplorhini and Strepsirhini lineages - a roughly 2-5 million year period (depending on who is telling the story). But then, after suffering such a significant structural upheaval, remained highly "conserved" for the next 60-or-so million years (while the rest of the genome evolved enough to make distinct species). I think multiple events over the short (evolutionary speaking) mutation period makes the story less believable. A gene with a function (i.e. a selective advantage) gets inactivated by mutation, but then, when the selective advantage is lost, the useless gene becomes strangely immune to large-scale mutations.

I agree it would be "interesting" to look into possible function(s) for GULOP, or even alternative functions for GULO. The Yang et.al. paper I provided shows how extensive the investigation would have to be to get funding. I would be surprised to find any such investigation dedicated to a single gene that has already been relegated to the trash. The Yang paper also demonstrates that you have to specifically look into the possibility before finding alternative activity. That's not been the order of investigation of GULOP. GULO genes were correlated to vitamin C synthesis, then, upon finding a putatively 'incomplete' GULO gene in animals that can't synthesise vitamin C, the 'incomplete' gene was relegated to the pseudogene pile. I'd be surprised if anyone has ever specifically researched the possibility of GULOP having a function.

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17 minutes ago, Tristen said:

I agree it would be "interesting" to look into possible function(s) for GULOP, or even alternative functions for GULO. The Yang et.al. paper I provided shows how extensive the investigation would have to be to get funding. I would be surprised to find any such investigation dedicated to a single gene that has already been relegated to the trash. The Yang paper also demonstrates that you have to specifically look into the possibility before finding alternative activity. That's not been the order of investigation of GULOP. GULO genes were correlated to vitamin C synthesis, then, upon finding a putatively 'incomplete' GULO gene in animals that can't synthesise vitamin C, the 'incomplete' gene was relegated to the pseudogene pile. I'd be surprised if anyone has ever specifically researched the possibility of GULOP having a function.

Sounds like a really good project for an AiG scientist.

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