Jump to content
one.opinion

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

Recommended Posts

Pseudogenes are sequences of DNA that share considerable resemblance ordinary genes (by examination of nucleotide sequence), but have either partially or completely lost function - essentially, they don't encode a functional protein product. Most of the roughly 13,000 pseudogenes in the human genome can be identified by finding very similar active gene sequences elsewhere in the genome, usually in close proximity. It is thought by most scientists that these pseudogenes arose by duplication and divergence, or accidental copying of an extra version, followed by mutations that result in loss of function. However, there are a much smaller number of "unitary pseudogenes" that do not have a functional "counterpart" within the genome. These unitary pseudogenes can be identified by observing DNA sequence similarity to functional genes in other organisms. One example of this in the human genome is the GULOP pseudogene, that shares considerable DNA sequence with GULO genes in other mammals. The functional GULO gene encodes the gulonolactone (-L) oxidase enzyme that is used to make vitamin C. Many animals, including most mammals, can make their own vitamin C using this gene instead of needing to acquire it through the diet like humans do. From a young earth creationist or intelligent design viewpoint, it seems rather odd for humans to have a non-functioning version of this gene present in our genomes. What is even more odd is that some of the critical mutations within the GULOP pseudogene are actually shared between humans and most other primates. The fact that this pseudogene is present in the human genome combined with the fact that this pseudogene shares these critical mutations in versions found in other primates seems to suggest our common biological ancestry. 

  • Thumbs Up 1

Share this post


Link to post
Share on other sites

Hi One,

It’s unfortunate that you haven’t provided any data to analyze, so I will have to focus my response on the assumptions evident in your position.

Pseudogenes are sequences of DNA that share considerable resemblance ordinary genes (by examination of nucleotide sequence), but have either partially or completely lost function - essentially, they don't encode a functional protein product.

So your first assumption is that pseudogenes don’t have a function. This is the same logical error you find in the vestigial organs and JunkDNA claims; i.e. that no known function equals no function.

As we have discussed previously with RNA, expression is a very complex issue. Some genes are only expressed during certain stages of development, others only expressed under certain environmental conditions. The expression of many genes are regulated epigenetically. It is impossible to know for certain that a sequence has no function.

it cannot be stated with certainty that a gene is unequivocally either a pseudogene or a gene. It is possible that analysis has not been performed in the appropriate temporo-spatial conditions to detect expression.

(http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(00)01199-6/epdf)

Therefore, any historical claim about a gene having “partially or completely lost function” is speculation based on the unverifiable premise that they are related due to their similarity, and that their lack of known function is a result of mutational error.

As an example of a violation of this assumption, Makorin1-P1 (a pseudogene of Makorin1) is saturated with mutational errors (insertions, deletions, substitutions etc.) – such that it should, by most conventional standards, have no function. And yet was found in repeatable experiments to regulate the decay of Makorin1 mRNA (https://www.nature.com/articles/nature01535).

This example raises the question of what we mean by function. I think creationists would generally agree that God would not place purposeless genes into the genome (though this too is an assumption). But even at a base level, transcribed pseudogenes can act as expression regulators (e.g. primer recruitment), RNA stabilizers/regulators and protein buffers (if translated). Whether or not such ‘functions’ are incidental or intentional cannot be empirically quantified, and must therefore be assumed on the basis of faith presupposition.

 

It is thought by most scientists that these pseudogenes arose by duplication and divergence, or accidental copying of an extra version, followed by mutations that result in loss of function.”

Having had similar conversations with me in the past, you should now understand that this is simply one interpretation of how the pseudogenes might have arisen. It’s a story generated by assuming a secular reality (with no involvement from God), then assuming that simple biotic life arose from abiotic chemical reactions, which subsequently evolved into complex life. Under that faith premise, multiple copies of the same gene must have arisen through mutational, transposition or duplication events (I haven't yet heard anyone argue for the convergent evolution of the same genes – which is the only other option under this paradigm).

However, if you start from the faith premise of a Designer, multiple genes could very well be an artifact of design – e.g. to facilitate the increased translation of a particular gene product when needed. So whether or not you accept the secular story is dependent upon whether or not you accept the secular premise upon which it is based.

 

From a young earth creationist or intelligent design viewpoint, it seems rather odd for humans to have a non-functioning version of this gene present in our genomes.

Loss of information mutations are entirely consistent with a very good creation suffering the decay brought on by human sin (assuming, of course, the gene has no function – i.e. is a true pseudogene).

 

What is even more odd is that some of the critical mutations within the GULOP pseudogene are actually shared between humans and most other primates. The fact that this pseudogene is present in the human genome combined with the fact that this pseudogene shares these critical mutations in versions found in other primates seems to suggest our common biological ancestry.

This 2003 study (https://www.jstage.jst.go.jp/article/jnsv1973/49/5/49_5_315/_pdf/-char/en) found that guinea pigs had the same mutation in the GULO pseudogene as humans – where more than a third of the “critical mutations” were shared between the two species. Yet the evolution story has primates (inc. those with working copies of the gene) as our closer, intermediate relatives. That is, the exact same inactivation sequence (in this case 47 nucleotides) of the gene must have occurred independently in both species. So such shared mutational ‘errors’, even under the Common Ancestor paradigm, do not “suggest our common biological ancestry” when considering the facts.

A high percentage of the same substitutions in the total substitutions (36%) indicates that there were many hot spots for nucleotide substitution throughout the sequences examined.

Assuming an equal chance of substitution throughout the sequences, the probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions and more was calculated to be 1.84X 10-12. This extremely small probability indicates the presence of many mutational hot spots in the sequences.

I don’t know what the GULO similarity mutation rate is between humans and the other primates you mention (since you haven’t provided that data), but this study shows that many “critical mutations” can be shared by divergent species in a manner that does not “suggest our common biological ancestry”. They are interpreted as evidence of “mutational hot spots” rather than indications of shared ancestry. Now I tend to agree with the latter interpretation – but notice how effortlessly they construct another story when the facts don’t match the Common Ancestry story. Shared errors means shared ancestry when the facts fit the story, but indicate mutational hot spots when the facts cannot be made to conform to the story.

 

 

  • Thumbs Up 1

Share this post


Link to post
Share on other sites

Hi Tristen, good to hear from you!

58 minutes ago, Tristen said:

So your first assumption is that pseudogenes don’t have a function.

What I said was pseudogenes "don't encode a functional protein product". There are a handful of exceptions (less than 20, if I'm remembering correctly) to this, but a vast majority of the ~13,000 pseudogenes in the human genome do not produce a functional protein product, while their "real gene" counterparts do. It is very reasonable to assume that these pseudogenes have indeed lost their original function. I don't know of any reports for a function of the GULOP pseudogene, but it may be possible to find reports for others. However, I would greatly hesitate to say that one or two examples of pseudogenes with an alternate function means that the remaining 13,000 do, as well.

1 hour ago, Tristen said:

it cannot be stated with certainty that a gene is unequivocally either a pseudogene or a gene. It is possible that analysis has not been performed in the appropriate temporo-spatial conditions to detect expression.

This is actually rather easy to demonstrate in the case of the GULOP pseudogene, since humans do not make ascorbic acid (vitamin C). If you assume that God created the pseudogene to LOOK a like the real GULO gene, but carry out a different function, then we run into the long standing question of "Why would God create such a deception"?

1 hour ago, Tristen said:

As an example of a violation of this assumption, Makorin1-P1 (a pseudogene of Makorin1) is saturated with mutational errors (insertions, deletions, substitutions etc.) – such that it should, by most conventional standards, have no function. And yet was found in repeatable experiments to regulate the decay of Makorin1 mRNA (https://www.nature.com/articles/nature01535).

This is indeed an interesting example. However, it is one example out of 13,000. There would need to be demonstrated functions for thousands more pseudogenes to suggest that they are not a result of accumulated mutations, rather than molecular happenstance.

1 hour ago, Tristen said:

Having had similar conversations with me in the past, you should now understand that this is simply one interpretation of how the pseudogenes might have arisen. It’s a story generated by assuming a secular reality (with no involvement from God), then assuming that simple biotic life arose from abiotic chemical reactions, which subsequently evolved into complex life.

True, this is one interpretation, but it is the interpretation supported by evidence. Duplications of DNA sequences occur on a regular basis. Mutations also occur on a regular basis. The GULO gene in mice is over 22,000 nucleotides long, and there are high degrees of similarity between the mouse GULO and the human GULOP. It is very reasonable to conclude that the GULOP is a deteriorated version of the functional GULO gene.

This is probably also a good place to remind readers that it is entirely possible to be a child of God and co-heir with Christ and accept evolution as the work of His hands. So it's a bit of a misrepresentation (intentionally or unintentionally) to say "It’s a story generated by assuming a secular reality (with no involvement from God)".

1 hour ago, Tristen said:

This 2003 study (https://www.jstage.jst.go.jp/article/jnsv1973/49/5/49_5_315/_pdf/-char/en) found that guinea pigs had the same mutation in the GULO pseudogene as humans – where more than a third of the “critical mutations” were shared between the two species. Yet the evolution story has primates (inc. those with working copies of the gene) as our closer, intermediate relatives. That is, the exact same inactivation sequence (in this case 47 nucleotides) of the gene must have occurred independently in both species. So such shared mutational ‘errors’, even under the Common Ancestor paradigm, do not “suggest our common biological ancestry” when considering the facts.

It is true that guinea pigs and humans share some point mutations. However, what I was referring to was the loss of entire exons (regions of genes responsible for the actual protein coding). The paper you kindly provided shows that the rat version of the GULO contains 12 exons. The guinea pig version is missing only exons 1 and 5. Humans are missing exons 1, 2, 3, 5, 6, 8, and 11. The missing exons will have a much greater impact than single nucleotide substitutions, and show a clear distinction between the guinea pig and human versions. It is misleading to use the nucleotide similarities to claim similarity while the exons are so different. So back to the suggestion of common biological ancestry - chimps, bonobos, orangutans, gibbons, and quite a few other primates also cannot synthesize vitamin C. I don't believe it is coincidental that exons 1, 2, 3, 5, 6, 8, and 11 are also missing from EACH of the GULOP versions in these other primates.

  • Thumbs Up 1

Share this post


Link to post
Share on other sites
2 hours ago, one.opinion said:

Hi Tristen, good to hear from you!

What I said was pseudogenes "don't encode a functional protein product". There are a handful of exceptions (less than 20, if I'm remembering correctly) to this, but a vast majority of the ~13,000 pseudogenes in the human genome do not produce a functional protein product, while their "real gene" counterparts do. It is very reasonable to assume that these pseudogenes have indeed lost their original function. I don't know of any reports for a function of the GULOP pseudogene, but it may be possible to find reports for others. However, I would greatly hesitate to say that one or two examples of pseudogenes with an alternate function means that the remaining 13,000 do, as well.

This is actually rather easy to demonstrate in the case of the GULOP pseudogene, since humans do not make ascorbic acid (vitamin C). If you assume that God created the pseudogene to LOOK a like the real GULO gene, but carry out a different function, then we run into the long standing question of "Why would God create such a deception"?

This is indeed an interesting example. However, it is one example out of 13,000. There would need to be demonstrated functions for thousands more pseudogenes to suggest that they are not a result of accumulated mutations, rather than molecular happenstance.

True, this is one interpretation, but it is the interpretation supported by evidence. Duplications of DNA sequences occur on a regular basis. Mutations also occur on a regular basis. The GULO gene in mice is over 22,000 nucleotides long, and there are high degrees of similarity between the mouse GULO and the human GULOP. It is very reasonable to conclude that the GULOP is a deteriorated version of the functional GULO gene.

This is probably also a good place to remind readers that it is entirely possible to be a child of God and co-heir with Christ and accept evolution as the work of His hands. So it's a bit of a misrepresentation (intentionally or unintentionally) to say "It’s a story generated by assuming a secular reality (with no involvement from God)".

It is true that guinea pigs and humans share some point mutations. However, what I was referring to was the loss of entire exons (regions of genes responsible for the actual protein coding). The paper you kindly provided shows that the rat version of the GULO contains 12 exons. The guinea pig version is missing only exons 1 and 5. Humans are missing exons 1, 2, 3, 5, 6, 8, and 11. The missing exons will have a much greater impact than single nucleotide substitutions, and show a clear distinction between the guinea pig and human versions. It is misleading to use the nucleotide similarities to claim similarity while the exons are so different. So back to the suggestion of common biological ancestry - chimps, bonobos, orangutans, gibbons, and quite a few other primates also cannot synthesize vitamin C. I don't believe it is coincidental that exons 1, 2, 3, 5, 6, 8, and 11 are also missing from EACH of the GULOP versions in these other primates.

What I said was pseudogenes "don't encode a functional protein product". There are a handful of exceptions (less than 20, if I'm remembering correctly) to this, but a vast majority of the ~13,000 pseudogenes in the human genome do not produce a functional protein product, while their "real gene" counterparts do.”

If there is even one example of a functional pseudogene (protein-coding or not) then the assumption that any pseudogene results from a broken “real gene” is unreliable. It doesn’t matter how many other pseudogenes we don’t know a function for. The ones where we do know their function, we originally didn’t know their function – until we did.

 

It is very reasonable to assume that these pseudogenes have indeed lost their original function.

Yes. But it remains an assumption. My position has no problem with the existence of true pseudogenes. But neither does my position assume that no known function should obligate the interpretation of a broken “original function” with similarities between species exclusively indicative of shared ancestry.

 

This is actually rather easy to demonstrate in the case of the GULOP pseudogene, since humans do not make ascorbic acid (vitamin C)

It only demonstrates that the gene called GULOP doesn’t make Vitamin C. It doesn’t demonstrate that the gene is derived from an originally working GULO gene inherited from a common ancestor. Nor does it demonstrate that it's not designed to do something else. Note: I’m not arguing for this – I have no problem with GULOP being a broken GULO, but you don’t seem to recognize the magnitude of the assumptions you are reading into the facts.

 

If you assume that God created the pseudogene to LOOK a like the real GULO gene, but carry out a different function, then we run into the long standing question of "Why would God create such a deception"?

I respectfully think this is nonsense. If a gene has a function, then it was designed to perform that function. Structural similarities to other genes are incidental. They “LOOK” Like what they are.

 

However, it is one example out of 13,000. There would need to be demonstrated functions for thousands more pseudogenes to suggest that they are not a result of accumulated mutations, rather than molecular happenstance.”

This is a Marginalization fallacy. I only need one example of a functional pseudogene to completely undermine the claim that described pseudogenes should be generally considered useless. You have 13,000 supposed examples of genes for which there is no known function. I have at least one example of an alleged pseudogene for which there is a known function.

It’s also a Strawman in the sense that I did not claim pseudogenes are “molecular happenstance”. I have no issue with pseudogenes arising from “mutations”. My issue is with you treating assumptions as fact – then building your argument on the supposed premise of that ‘fact’.

 

it is the interpretation supported by evidence. Duplications of DNA sequences occur on a regular basis. Mutations also occur on a regular basis.”

When talking about the origin of these genes, which interpretation is better “supported by evidence” is a matter of bias. Yes, duplication and other mutations have been observed. But that doesn’t justify a claim that a specific pseudogene arose from duplication, followed by mutation. You are assuming the history based on presupposition, not observing it. You are first assuming he secular evolution story is correct, then accepting another story about the origin of pseudogenes that conforms to the original story.

If the Biblical story, as portrayed in Genesis, is true, then the whole premise of the secular account is undone; God designed genes into the genome in whatever copy numbers He saw fit. Some may have since become corrupted beyond usefulness, others, we have yet to discover their function. The facts are that there are genes with no known function, that look similar to known functional genes. That’s all. Where they came from is a matter of interpretation – regardless of empty rhetorical platitudes about one being “supported by evidence”.

 

The GULO gene in mice is over 22,000 nucleotides long, and there are high degrees of similarity between the mouse GULO and the human GULOP. It is very reasonable to conclude that the GULOP is a deteriorated version of the functional GULO gene.”

But then you go on to say that the human version is missing 7 of the 12 exons found in mouse GULO. Tat's a stupendous difference. You can’t have it both ways.

And again, I have no problem with GULOP being a broken GULO. But you are trying to argue that common mutations speak to shared ancestry. The paper I presented demonstrated that only to be the case when convenient.

 

It is true that guinea pigs and humans share some point mutations.

So many, in fact, that the study mathematically demonstrated (and made a big deal about) the implausibility of such similarities arising through random mutations in such disparate species. Such similarities cannot, even under the secular paradigm, be applied to shared ancestry. Therefore they concluded that the uncanny similarities represented mutational hot spots, rather than shared ancestry.

 

However, what I was referring to was the loss of entire exons (regions of genes responsible for the actual protein coding). The paper you kindly provided shows that the rat version of the GULO contains 12 exons. The guinea pig version is missing only exons 1 and 5. Humans are missing exons 1, 2, 3, 5, 6, 8, and 11. The missing exons will have a much greater impact than single nucleotide substitutions, and show a clear distinction between the guinea pig and human versions. It is misleading to use the nucleotide similarities to claim similarity while the exons are so different.”

Your original statement said nothing about lost exons. You just said that shared “critical mutations” “suggest our common biological ancestry”. I presented a paper showing your reasoning to be untenable in light of the facts – i.e. that shared “critical mutations” can arise en masse, independently of shared ancestry. So there was nothing “misleading” in anything I said. You are the only one who has claimed genetic similarity (in mutations) suggests shared ancestry. That’s the premise of the opening post.

 

So back to the suggestion of common biological ancestry - chimps, bonobos, orangutans, gibbons, and quite a few other primates also cannot synthesize vitamin C. I don't believe it is coincidental that exons 1, 2, 3, 5, 6, 8, and 11 are also missing from EACH of the GULOP versions in these other primates.”

What’s it gonna take to get a look at your supporting data? Or do I have to take your word for it.

 

 

  • Thumbs Up 1

Share this post


Link to post
Share on other sites
21 minutes ago, Tristen said:

If there is even one example of a functional pseudogene (protein-coding or not) then the assumption that any pseudogene results from a broken “real gene” is unreliable. It doesn’t matter how many other pseudogenes we don’t know a function for. The ones where we do know their function, we originally didn’t know their function – until we did.

 

32 minutes ago, Tristen said:

This is a Marginalization fallacy. I only need one example of a functional pseudogene to completely undermine the claim that described pseudogenes should be generally considered useless.

This is incorrect. Your logic is similar to someone combing through a pile of 13,000 forks, finding a spoon, and claiming that the remaining 12,999 are therefore not forks.

Olfactory genes are notorious as a source of material for the production of pseudogenes. Here is an interesting article on a "pseudo pseudogene" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164928/), but that doesn't mean that the hundreds of other nonfunctioning derivatives of the olfactory genes have an undiscovered function.

46 minutes ago, Tristen said:

When talking about the origin of these genes, which interpretation is better “supported by evidence” is a matter of bias. Yes, duplication and other mutations have been observed. But that doesn’t justify a claim that a specific pseudogene arose from duplication, followed by mutation. You are assuming the history based on presupposition, not observing it. You are first assuming he secular evolution story is correct, then accepting another story about the origin of pseudogenes that conforms to the original story.

The fact that duplication and mutation occur suggests that combining the two can result in the production of pseudogenes. When the pseudogenes contain long stretches of high nucleotide similarity to the functioning gene, it isn't difficult to put 2+2 together.

1 hour ago, Tristen said:

But then you go on to say that the human version is missing 7 of the 12 exons found in mouse GULO. Tat's a stupendous difference. You can’t have it both ways.

It isn't difficult to see how both can be true. In the exons that are shared, there is considerable nucleic acid similarity.

1 hour ago, Tristen said:

So many, in fact, that the study mathematically demonstrated (and made a big deal about) the implausibility of such similarities arising through random mutations in such disparate species. Such similarities cannot, even under the secular paradigm, be applied to shared ancestry. Therefore they concluded that the uncanny similarities represented mutational hot spots, rather than shared ancestry.

5 hours ago, Tristen said:

A high percentage of the same substitutions in the total substitutions (36%) indicates that there were many hot spots for nucleotide substitution throughout the sequences examined.

 

Assuming an equal chance of substitution throughout the sequences, the probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions and more was calculated to be 1.84X 10-12. This extremely small probability indicates the presence of many mutational hot spots in the sequences.

I was going to let this slide after your first post, but since you've referred to it again, I'm not finding these quotes in the paper you provided earlier. Where did they come from? In any case, the case for shared ancestry is through the loss of exons, not the point mutations, that would have considerable less effect on gene function.

1 hour ago, Tristen said:

Your original statement said nothing about lost exons.

Yes, my OP did not mention the exons because I was attempting to avoid getting too far into the scientific jargon. Perhaps that was a mistake.

1 hour ago, Tristen said:

So there was nothing “misleading” in anything I said.

The data showing the loss of exons was easily observed in the paper you provided. The omission of the exon info, and suggesting the human GULOP and guinea pig GULOP were very similar was misleading, albeit unintentional.

1 hour ago, Tristen said:

What’s it gonna take to get a look at your supporting data?

Well, you could start with the article you provided. Then you can read on here - The Genetics of Vitamin C Loss in Vertebrates

  • Thumbs Up 1

Share this post


Link to post
Share on other sites
18 hours ago, one.opinion said:

 

This is incorrect. Your logic is similar to someone combing through a pile of 13,000 forks, finding a spoon, and claiming that the remaining 12,999 are therefore not forks.

Olfactory genes are notorious as a source of material for the production of pseudogenes. Here is an interesting article on a "pseudo pseudogene" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164928/), but that doesn't mean that the hundreds of other nonfunctioning derivatives of the olfactory genes have an undiscovered function.

The fact that duplication and mutation occur suggests that combining the two can result in the production of pseudogenes. When the pseudogenes contain long stretches of high nucleotide similarity to the functioning gene, it isn't difficult to put 2+2 together.

It isn't difficult to see how both can be true. In the exons that are shared, there is considerable nucleic acid similarity.

I was going to let this slide after your first post, but since you've referred to it again, I'm not finding these quotes in the paper you provided earlier. Where did they come from? In any case, the case for shared ancestry is through the loss of exons, not the point mutations, that would have considerable less effect on gene function.

Yes, my OP did not mention the exons because I was attempting to avoid getting too far into the scientific jargon. Perhaps that was a mistake.

The data showing the loss of exons was easily observed in the paper you provided. The omission of the exon info, and suggesting the human GULOP and guinea pig GULOP were very similar was misleading, albeit unintentional.

Well, you could start with the article you provided. Then you can read on here - The Genetics of Vitamin C Loss in Vertebrates

This is incorrect. Your logic is similar to someone combing through a pile of 13,000 forks, finding a spoon, and claiming that the remaining 12,999 are therefore not forks.”

This is a false analogy. In our discussion, you are arguing on the basis of 13000 non-facts (i.e. no known function). I am arguing on the basis of fact (known/observed function).

 

Olfactory genes are notorious as a source of material for the production of pseudogenes. Here is an interesting article on a "pseudo pseudogene" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164928/), but that doesn't mean that the hundreds of other nonfunctioning derivatives of the olfactory genes have an undiscovered function.”

I have stated several times that I have no problem whatsoever with the existence of true pseudogenes. However, your story of how pseudogenes arose, underpinning you’re your interpretation of shared ancestry, relies on assuming no known function equals no function.

So your argument (as I understand it in the opening post) is; given the assumption that described pseudogenes are leftovers from working, functional genes, and have no inherent function of their own, and given that described pseudogenes only arise through duplication and mutation events (as opposed to being corruptions of God-designed genes), then it is extremely unlikely that separate species would share complex mutation patterns apart from inheritance via a shared ancestor.

The existence of functions found for pseudogenes undermines any obligation to the assumption that no known function means no function (which was logically specious without this evidence). So you can no longer automatically assume anything labelled a pseudogene is a non-functional leftover from some previously working gene - just because a function hasn't, to-date, been characterised. If a gene is shown to be functional, it can just as well be interpreted a designed variant of the homolog, rather than a "derivative" of a previous version of a "real" gene. Unless the mutation is observed, you can't assume one version of its history is more valid than another - regardless of whether a function has been described or not.

I am glad the article uses properly hedged language. "no clear functions for pseudogene-derived proteins are known". I am perfectly happy with that assessment.

 

The fact that duplication and mutation occur suggests that combining the two can result in the production of pseudogenes.”

Right - observations of duplication and mutation give the story plausibility. But they don't add any weight of evidence to the claim that that's how these pseudogenes actually arose - i.e. they don't make that story any more plausible than the story of God designing functional genes which have subsequently been corrupted. It always comes back to the faith presupposition through which we interpret the facts.

 

When the pseudogenes contain long stretches of high nucleotide similarity to the functioning gene, it isn't difficult to put 2+2 together.”

See above answer.

Gene duplication + mutations = pseudogenes

OR

God-designed genes + mutational corruptions = pseudogenes

The common fact is pseudogenes. But which version of the pseudogene's history you prefer is dependent upon presupposition.

 

It isn't difficult to see how both can be true. In the exons that are shared, there is considerable nucleic acid similarity.”

You used the same facts to argue they are too similar and too different at the same time. Appealing to similarity makes your argument the same as any homologous gene - which has not been the topic of this discussion. Your original argument had nothing to do with general "nucleic acid similarity", but specifically the similarity of "critical mutations" found in pseudogenes between species.

 

“I was going to let this slide after your first post, but since you've referred to it again, I'm not finding these quotes in the paper you provided earlier. Where did they come from?

I don’t expect you to let anything “slide”. If I forget to reference a quote (or paste the wrong link) then I am more than happy for you to require clarification. In this case the reference link is;

https://www.jstage.jst.go.jp/article/jnsv1973/49/5/49_5_315/_pdf/-char/en

The first quote is from the second page of the article (pg 316), i.e. underneath Figure 1, second column, middle paragraph, last sentence.

The second quote is found on the next page (pg 317) in the end of the label description for Figure 2.

 

In any case, the case for shared ancestry is through the loss of exons, not the point mutations, that would have considerable less effect on gene function.”

That was not your argument. Your original argument (i.e. the argument to which I was responding) was that common "critical mutations" in pseudogenes shared between species is indicative of shared ancestry. I provided a paper showing that large scale, shared mutations in pseudogenes (in particular GULO) can arise independently of shared ancestry. When the data didn't plausibly fit the secular story, a different interpretation for shared mutations (other than shared ancestry) was generated.

 

Yes, my OP did not mention the exons because I was attempting to avoid getting too far into the scientific jargon. Perhaps that was a mistake

Making broad, unsupported claims is always going to be problematic when dealing with people who think for themselves. Otherwise, you are expecting people holding an opposing position to simply take your word for any claim you make. That defies any expectation of critical reasoning; which is especially pertinent in a debate over scientific issues.

 

The data showing the loss of exons was easily observed in the paper you provided. The omission of the exon info, and suggesting the human GULOP and guinea pig GULOP were very similar was misleading, albeit unintentional.”

No reference system ever, has ever required the referencer to list all the ancillary facts found on a referenced paper – in the off chance that someone might find them pertinent. That would be both redundant and absurd. I hope your attempt to hold me to such a ridiculous standard (or else accusing me of being “misleading”) isn’t an indication that you are planning to revert to that ‘dishonest creationist’ nonsense we’ve discussed in other conversations.

The point of referencing is to provide source support for specific claims. The specific claim I made was that, even under the secular paradigm, complex mutation patterns can arise in disparate species in a manner that can’t be explained by inheritance through shared ancestry. The paper I provided made that explicit point in comparing the guinea pig GULO to the human GULO.

I did not suggest “the human GULOP and guinea pig GULOP were very similar”. I stated that they share a mutational haplotype defined by, to quote myself, “(in this case 47 nucleotides)” – which cannot be plausibly explained (according to the authors of the research) by inheritance through shared ancestry. I was very specific about my claim.

The exon data you defer to actually adds weight to my claim, as it shows how different the species are from each other. But since neither of us is claiming they are closely related, that information is largely irrelevant.

 

Well, you could start with the article you provided. Then you can read on here - The Genetics of Vitamin C Loss in Vertebrates

The article I provided only compared rat, guinea pig and human GULO. The article you provided claims that “The GLO gene of anthropoid primates has lost seven of the twelve exons found in functional vertebrate GLO genes”, and provides a nice figure to that effect (i.e. fig. 4), but the references provided only support the claim that these exons are lost in humans. Reference 31 looked at 4 primates, but only a 164nt sequence in exon X. Reference 30 only compared the human against the rat GULO. They seem to be basing this claim (for all “anthropoid primates”) on the following statement (from ref. 30), which just assumes the same loss of exons must be the reason for GULO inactivation observed across these primates;

Since both New World and Old World monkeys are deficient in GLO, whereas prosimians possess this enzyme (14), the loss of GLO in primates is thought to have occurred before the divergence of New World monkeys and Old World monkeys (35-45 million years ago) and after the divergence time of the prosimian and simian lineages (50-65millionyearsago).”

What I am after is the actual study showing all these primates lack the same exons (since that is now your argument). I already have an answer, but I would feel a bit silly explaining something that may not be true.

The article did tell an interesting story with the fish. The GULO gene is presumed (under the secular evolution paradigm) to have arisen in or before the existence of early vertebrates – except that there is no trace of it to be found in teleost fish. That doesn’t fit well with the “established” evolution story. This gene must have been “lost in the common ancestor of teleost fish”. You see, what happened is, there was a “complete loss of the GLO gene because BLAST searches cannot identify GLO gene sequences in any of the completely sequenced teleost fish genomes”. “Given the high degree of conservation of this gene, the fact that GLO orthologues cannot be identified from the currently available teleost genomes is likely the result of the fact that this non-functional gene has mutated beyond recognition or that it has been deleted from teleost genomes altogether”. It doesn’t fit the evolution story, which demands that all vertebrates have some remaining trace of the GULO gene, so mutations must have made it disappear. How did we ever explain anything without the magic of mutation?

  • Haha 1

Share this post


Link to post
Share on other sites
3 hours ago, Tristen said:

This is a false analogy. In our discussion, you are arguing on the basis of 13000 non-facts (i.e. no known function). I am arguing on the basis of fact (known/observed function).

The alternate activity of a tiny fraction of pseudogenes cannot be used as proof that all pseudogenes have an alternative function. It is indeed a fact that pseudogenes do not have the same function as the genes they so closely resemble. A very large percentage have no observable function at all.

Let’s try another analogy. If I see a Rembrandt and a smudged painting with clear similarity to the same Rembrandt, it would be my conclusion that something happened to mess up the smudged one, rather than assuming that Rembrandt painted them both in their existing conditions. One does not have to work from an atheistic assumption to conclude that pseudogenes are “smudged” version of original, functional genes. The conclusion is a plausible (and most plausible, in my opinion) explanation of observed fact.

(More later, time permitting, must sign off for now)

  • Thumbs Up 1

Share this post


Link to post
Share on other sites
3 hours ago, one.opinion said:

The alternate activity of a tiny fraction of pseudogenes cannot be used as proof that all pseudogenes have an alternative function. It is indeed a fact that pseudogenes do not have the same function as the genes they so closely resemble. A very large percentage have no observable function at all.

Let’s try another analogy. If I see a Rembrandt and a smudged painting with clear similarity to the same Rembrandt, it would be my conclusion that something happened to mess up the smudged one, rather than assuming that Rembrandt painted them both in their existing conditions. One does not have to work from an atheistic assumption to conclude that pseudogenes are “smudged” version of original, functional genes. The conclusion is a plausible (and most plausible, in my opinion) explanation of observed fact.

(More later, time permitting, must sign off for now)

The alternate activity of a tiny fraction of pseudogenes cannot be used as proof that all pseudogenes have an alternative function.

So it seems like I need to make this caveat every post – I have absolutely no problem with the existence of true pseudogenes. My position does not need to claim that “all pseudogenes have an alternative function”. And I certainly wouldn't use the term “proof” in any scientific discussion (except to refute the validity of its use).

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.

Your argument needs the genes to be non-functional to make that case. And so you have to assume that no known function equals no function. Your argument stands or falls on that assumption. The existence of functions in designated pseudogenes means no one is obligated to that assumption (besides the fact that the logic of the assumption is flawed – even in the absence of such evidence).

 

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.

 

Let’s try another analogy.

Oh joy.

 

One does not have to work from an atheistic assumption to conclude that pseudogenes are “smudged” version of original, functional genes.

Hmmmm. I (a young-earth, Biblical creationist) have absolutely no problem with the existence of true pseudogenes.

 

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.

 

  • Thumbs Up 1

Share this post


Link to post
Share on other sites
On ‎11‎/‎28‎/‎2017 at 10:35 AM, one.opinion said:

The fact that this pseudogene is present in the human genome....
combined with the fact that this pseudogene shares these critical mutations....
in versions found in other primates seems to suggest our common biological ancestry.... 

:)

You Are Getting Sleepy
Sleepy Sleepy
Sleepy

O Timothy, keep that which is committed to your trust, avoiding profane and vain babblings, and oppositions of science falsely so called: 1 Timothy 6:20 (American King James Version)

If you look for truth, you may find comfort in the end; if you look for comfort you will not get either comfort or truth only soft soap and wishful thinking to begin, and in the end, despair. https://www.brainyquote.com/quotes/c_s_lewis_141015

~

On ‎11‎/‎30‎/‎2017 at 4:48 PM, Tristen said:

I am glad the article uses properly hedged language....
"no clear functions for pseudogene-derived proteins are known"....
I am perfectly happy with that assessment....

Making broad, unsupported claims is always going to be problematic....
when dealing with people who think....
for themselves.... 

How did we ever explain anything....
without the magic of mutation....

:sherlock:

Without

Then God said, "Let there be lights in the sky to separate the day from the night. They will be signs and will mark religious festivals, days, and years. They will be lights in the sky to shine on the earth." And so it was. God made the two bright lights: the larger light to rule the day and the smaller light to rule the night. He also made the stars. God put them in the sky to give light to the earth, to dominate the day and the night, and to separate the light from the darkness. God saw that it was good. There was evening, then morning-a fourth day. Genesis 1:14-19 (GOD'S WORD® Translation)

The Magic

The LORD merely spoke, and the heavens were created. He breathed the word, and all the stars were born. Psalms 33:6 (New Living Translation)

Of Evolution

Thou art worthy, O Lord, to receive glory, and honor, and power: for thou hast created all things, and for thy pleasure they are and were created. Revelation 4:11 (Webster Bible Translation)

~

Be Blessed Beloved Of The KING

The LORD bless thee, and keep thee:
The LORD make his face shine upon thee, and be gracious unto thee:
The LORD lift up his countenance upon thee, and give thee peace.
And they shall put my name upon the children of Israel; and I will bless them. Numbers 6:24-27 (King James Bible)
 
Love, Your Brother Joe
 
~
 
Thy word is true from the beginning: and every one of thy righteous judgments endureth for ever. Psalms 119:160 (King James Bible)
 
The Bible contains the mind of God, the state of man, the way of salvation, the doom of sinners, and the happiness of believers. Its doctrines are holy, its precepts are binding, its histories are true, and its decisions are immutable.
 
Read it to be wise, believe it to be safe, and practice it to be holy. It contains light to direct you, food to support you, and comfort to cheer you.
 
It is the traveler’s map, the pilgrim’s staff, the pilot’s compass, the soldier’s sword and the Christian’s charter. Here too, Heaven is opened and the gates of Hell disclosed.
 
Christ is its grand subject, our good its design, and the glory of God its end. It should fill the memory, rule the heart and guide the feet. Read it slowly, frequently and prayerfully.  It is a mine of wealth, a paradise of glory, and a river of pleasure.
 
It is given you in life, will be opened at the judgment, and be remembered forever. It involves the highest responsibility, rewards the greatest labor, and will condemn all who trifle with its sacred contents.
 
From The Inside Of My Gideon New Testament

Share this post


Link to post
Share on other sites
1 hour ago, FresnoJoe said:

Of Evolution

Thou art worthy, O Lord, to receive glory, and honor, and power: for thou hast created all things, and for thy pleasure they are and were created. Revelation 4:11 (Webster Bible Translation)

Hi Joe, thanks for your input. For the record, I am 100% in agreement that God is the Creator and Sustainer of all things. It jus happens that Tristen and I disagree on the details of how He performed His creative work.

  • Thumbs Up 1

Share this post


Link to post
Share on other sites

×