You do realize that just because you can IMAGINE why hundreds of data points are wrong doesn’t place an obligation on your readers to think your conclusions are valid, right?
I can’t list all the times that I (or others) have presented the cumulative aggregation of perhaps 200 significant flaws or indicators regarding the flawed historicity of the Bible.
Evangelicals dutifully present their “cherry picked” explanation for each of these 200 (or more issues).
But at the end of the day, no objective observer thinks an ancient text can have dozens OF DOZENS of reporting problems and STILL think it is definitively reliable.
We can tell that the human VIT pseudogene fragments cannot be translated into VIT proteins - the fragments are small, and even those remaining fragments are riddled with mutations that would prevent their translation. The minute amount of yolk in placental mammals thus cannot come from these sequences.
Thanks Dennis! That helps…playing devils advocate though, and I’ve heard this mentioned elsewhere before, can’t even fragmented genes that are incapable of producing full contiguous proteins still transcribe amino acids or truncated chains? Is it outside the realm of possibility that such products could serve a nutrietive role in lieu of a full yolk for an embryo? Thanks!
There are rare cases of RNA editing that may do something like this for some loci, but the VIT fragments in the human genome are so far gone that there’s no way RNA editing could “rescue” them. There is very little of these genes left.
Thanks Dennis. This makes a lot of sense. But following this line of reasoning, doesn’t this point hold true for most any severely degraded pseudogene? But for some reason none of the other examples out there seem to be compelling to creationists. I, perhaps like you, thought the vitellogenin pseudogenes would be more convincing for the fact that humans have no need for yolk production. But if the point is conceded that there are minuscule amounts of yolk-like nutrients produced in the embryo, then we lose some of the power of that point. And while mentioning that the gene is far too degraded to produce any protein needed to manufacture said yolk-like substances is valid, this is no different than mentioning the same thing about for instance a severely degraded olfactory pseudogene. So what then is unique about this example that makes it more compelling? Thanks!
Vitellogenins are the genes used for bulk yolk transfer in egg-laying organisms. The minuscule amount of yolk found in placentals is not VIT based. So, there is no reason, from a antievolutionary perspective, to find VIT sequences in placental mammals, since placentals have no need for bulk yolk transfer. Evolution, however, predicts that placental mammals are descended from egg-laying ancestors, and thus may retain fragments of the VIT genes harkening back to that former way of life. If so, these fragments should be in blocks of syntenty conserved with egg-laying vertebrates. So, what we observe in placentals is exactly what evolution would predict.
Thanks Dennis. But I thought that VIT genes are for both the production of yolk and its bulk transfer from the liver to the oocyte? Am I wrong? Is the yolk produced elsewhere and the VIT genes then just transport it?
Hi Tim - vitellogenins are the main component of yolk in egg-laying organisms. They’re made by the mother, transported through the bloodstream, and are deposited as the egg yolk.
Placental “yolk” is made up of other proteins (not vitellogenins).
Thanks Dennis. By “placental yolk” do you mean the minuscule amounts of yolk present in the embryo or something else? Also, do you know what produces this? I’ve searched on my own and could never find it.
Thanks Dennis. But just playing through my head what a conversation with a creationist would look like, they’d say of course the mammalian “yolk” would not be produced by VIT genes, since we don’t see those genes in our genome anyway. But maybe by something with similarity to VIT genes, and then of course nominate what we call the VIT pseudogenes as a contender. Then we’re back to explaining this in more generic terms as to how pseudogenes don’t code for proteins and all that. But the uniqueness of “humans don’t need yolk” as a differentiator for this argument is lost. Unless we can one day find out what in fact does produce this mammalian “yolk.”
Well, you could point out that there are no genes in the human genome with similarity to VIT genes. That and you could point out that the VIT pseudogenes are so far gone, that not even young-earth creationists try to argue that they are somehow providing the minute amount of “yolk” placentals have.
Thanks Dennis. I think that could be helpful but could you elaborate on those points? The creationist could say that the VIT pseudogenes are similar enough to the VIT genes to produce mammalian “yolk.” If I then said, no, they’re not similar, then they could ask how have we arrived at the conclusion that they’re VIT pseudogenes at all? In which case no matter what I say I’ll be pointing to some similarity and then come across as if I’m contradicting myself. At which point the creationist will just laugh and consider me discredited. As to saying not even young-earth creationists argue that these could produce mammalian yolk, I’ve run across this very argument on at least a couple creationist sites. I referenced one. So I couldn’t make that argument as if a creationist ran across the same content online I did then they would also consider me discredited for saying that no such argument is being made when in fact it has. So I guess it hinges then on whether or not these VIT psuedogenes are so far past the gone in comparison to other pseudogenes that you’re looking at a slam-dunk argument that they are not functional in yolk production. How can I best articulate this case? And is this so vastly different than other pseudogenes we’ve seen advanced as arguments for common descent that are shrugged away by creationists?
In any event, you’d think that a research study (Biologos funded or in your lab?) could settle this to the satisfaction of any creationist committed, at least in principle, to some measure of intellectual honesty. If you could remove the VIT pseudogenes from say a rat genome, and validate that embryos produced lacking this component develop normally, you would have demonstrated the uselessness of this fossilized genetic relic. With all the effort and funds already expended to convince creationists of the reality of common descent/evolution, you’d think this effort could be well justified. What do you think?
The VIT pseudogenes in humans are not capable of being expressed as yolk genes. In order for a gene to function, it has to have numerous sequences that do certain jobs: a promoter sequence that tells the cell to start transcribing mRNA at a certain spot; within the mRNA, there needs to be a translation start sequence; the mRNA itself results from splicing out introns using specific splicing sequences; and the portion of the mRNA that has the coding sequence needs to have an uninterrupted run of codons that are intact, without a “stop codon” that tells the ribosome that it should cease translation. The VIT gene fragments in humans are defective in all of these requirements (and more).
The reason why we can recognize them is that despite these defects, some fragmentary remains of their sequences persist. These sequences, though fragmentary, match up with functional VIT sequences seen in other species and sit within conserved blocks of synteny, as the original post describes. There can be sufficient similarity to recognize the remains of these genes without those sequences having what is needed to be a functional gene. In fact, VIT pseudogene sequences could be almost identical to functional VIT genes but still be defective, if mutations were present that prevented gene function.
So, though the argument may be out there, it is not being made by anyone with an understanding of how genes work. Tomkins himself does not take that tack, because he knowns that argument is flawed.
As for doing a study to remove these sequences from a mammal, the experiment has already been done, as it were. “Removing” a gene is often done by introducing the exact sort of mutations into it that we already see in placental VIT sequences. Fully deleting a gene is not necessary to remove its function.
That’s a case where one short region of a vertebrate gene has relatively weak similarity to a small portion of an insect vitellogenin. If you go far back enough, yes, that sequence likely shares a common ancestral sequence with vitellogenins - but it’s not “a vitellogenin” - it’s a small portion of mildly VIT-like sequence used in another gene for a non-egg-laying function.
This is a case of “useful protein domains” being mixed and matched over evolutionary time. So, yes, point taken - there is one vertebrate gene with one domain with weak but significant similarity to a small portion of an invertebrate VIT gene. My point, in the context of Tim’s question, is that there are no genes in the human genome that act as VIT genes in the vertebrate sense of supplying egg yolk.
Just to point out the sloppiness of evolution, there are usually multiple translation start sequences; multiple splicing products, not all of which are functional; and of course an open reading frame is necessary, but a stop codon isn’t. Sometimes, read through is a feature, not a bug:
Thank you Dennis. I think that helps a lot. I know there is a lot of skepticism generally amongst creationists that pseudogenes are not “functional,” but it seems the excessively degraded nature of these genes with their missing so many necessary components for effective translation adds to the effectiveness of this example.
Regarding the experiment I suggested, however, no matter what argument we advance and not matter how otherwise convincing it ought by every right be, creationists will still hold out hope that there is some other function this genetic sequence may serve. And if we knock down argument after argument of the various functions they might propose, they will still just assume that there is some as of yet unidentified function that maybe requires a level of understanding that we do not yet possess. And they would likely apply the same expectation as to why the sequence shares similarity and synteny with yolk-producing genes when it has nothing to do with yolk production. They would claim that if we knew enough about the mysterious inner workings of our genetics an answer would suggest itself. By removing the sequence entirely, you nullify even that hope.
Is this something that is practically achievable for a geneticist such as yourself or an organization with the connections and funds of Biologos? Thanks Dennis!
