This is a companion discussion topic for the original entry at https://biologos.org/blogs/dennis-venema-letters-to-the-duchess/vitellogenin-and-common-ancestry-reading-tomkins
i dont think that the pseudo vit genes are evidence for a commondescent for 2 reasons:
1)the vit protein is a multifunctional. so even if it was active in humans it can function for other function then making yolk.
2)the fact that all those inactivation can happan convergently in many species (tooth loss for example happaned convergently about 10 times in 10 different species).
therefore a pseudo vit cant be consider as an evidence for a commondescent.
You’ve brought up these general points many times previously.
Explain your point #1.
A) How does multi-functionality affect arguments about common descent? What degree of ‘multifunctionality’ or partial reuse do you think is necessary to refute a claim of common descent? Could you work through the details and highlight the specific regions or ‘functions’ that you think support your claim?
B) At best, only a small section of the entirety of the vitellogenin remnant sequence has a role in an unrelated function in mammals. Do you understand that your statement might be considered a perfect example of the ‘missing the forest for the trees’ point that Dennis is making?
Explain your point #2,
A) In which species do you think vitellogenin was separately inactivated? What sort of patterns in the sequences would you expect to see if separate inactivation events occurred in various species? Consider addressing this both from the basis of a model of common descent and a model based on individual creation of ‘kinds’. You’ve seen the papers and have searched the literature on your own, now pull that information and synthesize a fuller argument: What sequence patterns would expect to find in today’s species if what your suggestion was true? Does the data match your expectations?
B) If you assume that the vitellogenin was inactivated ‘convergently’ in multiple species, aren’t you presuming that they once had a functional vitellogenin gene? Which mammalian species do you think ever had a working vitellogenin gene? It appears that most if not all mammals of today do not require a fully intact gene.
Consider the following question in your preferred model where animal ‘kinds’ are specially created: Why would a creator include functional vitellogenin in most mammalian ‘kinds’ when it is clear these kinds do not require it, and have inactivated the gene in similar ways? Does special creation make a good argument for what we observe?
I see the conversation is already underway, but as always I am available to answer questions.
The 150 base pair match on the VIT1 gene is not the evidence for common descent. 150 matches out of millions could be the result of random chance. The presence of other matching genes in that same general area, followed by the 150 matching base pairs in the same relative location where the VIT1 gene is placed in egg-laying species points very strongly to common descent.
Even if only that 150 base pair match was all that was left, even that would be enough to go on (if it was in the right genomic location). That level of matching goes far beyond what random chance will generate. So, even if we take Tomkins at face value - which we can’t as we have seen - he still can’t wave the evidence away.
On this or any other creationist critique of pseudogenes possessing “function” (though being reused and adapted for another purpose doesn’t make them not pseudogenes…but putting that aside for the moment), is there any way we can look to see if the genomes of other mammals have significant sections of the VIT pseudogenes or even all of them deleted? If they are truly and completely non-functional, would we expect this lack of conservation to occur over the length of time mammals have been on the scene? Or are deletions far rarer events than this and the “junk” keeps piling up? Thank you!
hey dennis. here is some interesting points:
- according to tomkins paper the 150 bp region is about 60% identical to the chicken one. its very conserve compare to the whole sequence (that have about 5% similarity with the chicken one). you dont think its possible that it indeed may have some function?
2)according to the paper monotremes diverged from other mammalian lines about 200 my ago. but the oldest monotreme fossil date about 110 my. its a 90 my gap between the molecular evidence and the fossil one.
Thieves remove 40÷ of the parts from my car’s engine. Can I still drive it?
Human engineering analogies often do not work with biology, but I think this one does.
the vit gene have other function then making yolk. so even if we go back to the evolution history we will find that this active gene actually doesnt have any conection to making yolk (its also answer to your second question part b).
any species that have stop codon\s in those genes. if we consider the vit as a real psrudogene.
see my 2 other points to prof venema.
With all due respect, dcsccc. Those aren’t really answers to my questions. I asked what sort of patterns would you expect to see if your assumptions were correct?
With regard to multi-functionality or past functions you have not addressed how the patterns are inconsistent with common descent. Additionally, you don’t address why these patterns of sequence similarities spread of over a large region of a chromosome make sense from a positive model of special creation. What design parameters must a creator operate with to specially create organisms in which the vitellogenin region would happen to exhibit sequence similarities to a different group like mammals? Why would a creator who individually made separate kinds deploy a pattern so consistent that we readily confuse it with common descent?
You replied that if vitellogenin was separately inactivated in multiple in multiple lines, you’d expect to see stop codons. No, not necessarily. ‘Stop’ codons are but one way of inactivating a gene. Deletions, inversions, insertions and knock-outs either in the transcribed region or outside can eliminated function.
Here’s the thing: If we compare the similar sequences that carry the vitellogenin region, we see that in mammals, it’s heavily ‘corrupted’. It’s not like a one or two mutations knocked out the gene but many. It’s as if most the mammals exhibit a similar degree of obliteration in that region. That’s not what you’d expect to see if the gene was active in all the mammalian kinds and was later, individually lost in each species. If the gene was recently active but now dead, there would be much less sequence divergence and fewer hits across the region.
I’m going to be out of town for awhile.
if it was similar in the first place (because of commondesigner)
according to this logic the tooth example also prove a commondescent (10 loss in 10 different species). but even in this case its not the result of commondescent. so why do you think that the vit example is a different case?
true. i actually do refer to deletions and insertions because they cause a stop codon. it can be any kind of bad mutation (even a whole exon loss).
why not actually? if this inactivation happaned very long time ago we will see this patern. even if they created by a designer in a speciel creation. on the other hand- evolution doesnt predict this either.
(In my response, I am using “unrelated” to mean “having no common ancestry.”)
My friend dcs, you seem very confused about how probability works in a stochastic process.
The overwhelming evidence is that DNA mutation is a stochastic, probabilistic process. Therefore, the theory that there a designer created different, unrelated species with a common gene, but that the mutations knocked out functionality in that gene in various species, would predict that the mutations would take different, unrelated forms in those various species.
The theory of common ancestry, on the other hand, would predict that the species that have a common ancestor would inherit mutations that are present in the genome of that common ancestor. Therefore, the mutations in these related species would be similar in form.
I am still astonished that you are still making this same fundamental mistake after months of discussion on this forum, no matter how frequently it gets pointed out to you.
Once again, I offer to help you (to the extent of my time availability) with problem sets from the free HarvardX courses on biostatistics. Contact me with a direct message if you are interested.
not true.they consider shared mutations as evidence for a commondescent. and non shared mutations as unique to the species. so its a circular reasoning.
What to you mean, “not true”? Are you suggesting that common ancestry does not lead to this prediction? If you are actually aiming to communicate that one of the standard and obvious predictions of evolutionary theory is just a muddled misunderstanding, then I’m afraid you will have to do so using more than a punchy “not true” and a single sentence containing two vagrant periods. I get aiming at concise, but overthrowing the bulk of modern science might require a little more legwork and sweat on the brow. Don’t worry, it’ll be well worth the effort when you get there;-)
The rest of your response is trying to be an argument, but it’s missing something (maybe a little, maybe a lot, I just can’t tell). How is it circular reasoning? The extensive pattern (and nested hierarchy) of shared mutations, as discussed above, is strong evidence for common descent while being a total mystery even for the wiliest baraminologist. I would love to hear a fleshed out (that is, multi-sentence) description of how this pattern is predicted from a YEC perspective. Maybe an argument can be made, but I haven’t heard it yet. The second part of your argument is that non-shared mutations are (usually) unique to the species. Ok. Yes, this is a reasonable explanation for non-shared mutations. Non-shared mutations are certainly explainable by both camps. This being the fairly obvious reason why non-shared mutations are not the focus of the discussion. Having figured out why this is a red herring that does not belong in this or any conversation of this type, let’s go back to your pending explanation of shared mutations. As others have pointed out above, you need to flesh out your theory, because no one seems to know how you come to the conclusion that YEC predicts what we see.
yep. evolution doesnt predict that two pseudogenes at 2 species must have the same mutations. you can always claim its the result of individual loss.
ok. so you are saying that creation model cant explain those shared mutations? can you give a specific example? thanks.
Individual loss? Out of curiosity, do you have an understanding of the probabilities involved here? To have not just one, but a pattern of shared pseudogene mutations for two species that are, by your account, unrelated? This time, more than one sentence is not needed, just yes or no, and a bit of explanation. If you have murky sense that it is not particularly likely that we end up with this pattern by chance, then good, it is a start, and you will at least have a sense of what you have to contend against. If you are able to get the sense that it is astronomically unlikely, then great, we are almost on the same page. If you don’t at all understand the probabilities involved, then at least be frank, and say that you’ve never really considered it. If you recognize that it is absurdly unlikely to get these results with separate creation, but you have an alternative explanation that can produce this same pattern over and over again, then please, go ahead, let’s hear it. I’ll repeat; “not true” is nice, but it doesn’t somehow make astronomical improbabilities disappear in a puff of smoke, it just means that you don’t understand or you don’t care about what is likely or unlikely when maintaining your position. Please try a bit harder to produce an argument. “No, I don’t really get the probabilities” would be fine; not understanding what is involved here but maintaining your position on faith would just mean you don’t have much to say on the subject and we can leave it at that.
You`re joking. You’d like me to offer a counter-example to an argument you haven’t made. DC, I have long understood that one of your tactics is answering questions with question or trying to pass the burden of the argument to the other person, but this just seems silly. If you can explain how special creation predicts these patterns as clearly as possible, I will try to help you out, but let’s not put the cart before the horse. In case that was not clear: you generally need to offer an actual explanation before anyone can know how to assess or refute that explanation in any way.
"Individual loss? Out of curiosity, do you have an understanding of the probabilities involved here? To have not just one, but a pattern of shared pseudogene mutations for two species that are, by your account, unrelated? "-
again- what is the problem? according to the data gorila and human shared about 15% of their genomes that doesnt shared with chimp. its mean that 1 in about 7 genes\pseudogenes in human and gorila shared mutations that chimp doesnt . so thousands bases are shared without a commondescent. therefore shared mutations cant be evidence for a commondescent. we can even arrange them in hierarchy for a specific gene- 1 mutation is shared between human gorila and chimp , and one is shared between gorila and human but not chimp.
dcs, you’ve had incomplete lineage sorting explained to you at least three times (that I am aware of). Those explanations seem to have had no effect on you.
Have you ever wondered why the pattern of relatedness between humans and other primates exactly matches the ILS pattern? Humans are the closest relatives to chimpanzees, then gorillas, then orang-utans. This pattern of relatedness predicts that humans will share the most ILS with gorillas and then orang-utans. Indeed, we were able to predict in advance how much ILS we expected in both cases, and the predictions matched up with the observed values very well.
As for probabilities, it’s not just mutations in two species you have to account for (not that your “explanation” for two species works). We see scores of shared mutations across many species (for example humans, chimpanzees, gorillas and orang-utans. Do you have a sense of how improbable it would be to have all of these mutations crop up independently in unrelated species, yet give a nested hierarchy pattern? Every mutation event is an extremely low probability event to begin with.
Evolution and the Gospel: From Enemy to Harmony
DC, since you already know all about ILS in great detail, I can’t imagine that this is anything more than an effort to distract from my requests for you to explain, using the creation model, why there is any pattern of shared mutations in pseudogenes at all if these species truly are unrelated. No, I don’t think you need ILS explained to you again and no, the distraction did not work. Please let’s move back to what has been repeatedly requested of you. I would appreciate it if you would explain your hypothesis as to how your model predicts such statistically unlikely results. Why should there be such a pattern of shared mutations at all if these species don’t share a common ancestor with this same pattern? Where does it come from? Or just say that you can’t explain it, which would be an acceptable, honest response. Honestly, there are very few options that I can picture for how to deal with this evidence from the YEC perspective, I’m just looking for some follow-through here.
I’ll note that the evasion (assuming this is what this last response was) might have actually worked if I hadn’t followed exactly those recent discussions where people kept explaining exactly this pattern (ILS) to you in careful and patient detail, including how and why it is predicted. At the very least, even if you did not understand a single one of those well-crafted explanations, you would be aware that there is an uncontroversial explanation available and you would no longer be in a position to act as though this was a contradiction to what is expected given common descent. This is the problem with posting for a long time on the same forum; (a) the repeated use of the same strategies become transparent and recognized after a while and (b) you can’t suddenly unknow something that you are known to know;-). If I am wrong, and you actually didn’t realize that ILS is the well known explanation of this pattern, then please tell me and although I will be bewildered, I will of course apologize for misreading your last comment.
I really do want to hear if there is a going YEC hypothesis designed to explain this pattern, and I frankly wouldn’t be surprised if there was just such an explanation (though I also wouldn’t be surprised if it fell apart when looked at the least bit closely). A bit like hydrological sorting in flood geology or different ecological zones leading to the vertical pattern of fossils in the geological column: absolutely awful explanations, but at least they threw something out there for anyone who just needed to hear that they had some kind of a response. I just haven’t seen this particular explanation yet in YEC writings and I’m hoping to engage with it if it exists. The Vitellogen paper (the original) being discussed above is actually the most direct YEC response that I have ever seen on this kind of issue, and now that it is being dismantled so easily, it is proving to be a huge disappointment for me (weirdly, a part of me is rooting for them when they make these efforts). I actually expected better from AiG, I really took it at face value when they told me that the 150 bp sequence was all there was to it. The reason why I am interested in seeing a genuine creationist response to these arguments is that I look at this sort of genetic evidence as being powerful and conclusive, and I find that the “not true” responses and the transparent evasions that are common in YEC circles do a great disservice to any honest dialogue between the positions.