Can you make a case that selection was involved in 10k splicing variants?
In a previous post, you wrote:
âYou have not shown anything close the limit Behe has set. His claim is that Darwinian process can explain differences up to the genus level.â
Are you saying that you donât agree with Behe?
What challenge? If alternative splice events produce non-functional proteins it isnât a problem because the functional protein is still being produced.
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The fact some variants work better than others is evidence they will be subject to selection. Thatâs how evolution works Bill. Differential reproductive success. That you still donât understand the very basics of the thing youâre railing against is truly pathetic.
I donât understand this comment. No one has made that canât evolve claim.
So you can show these proteins are non functional?
This is not the question. You need to reconcile 10k selected variants over 6 to 10 million years in order to support your claim. Just repeating the selection mantra is not a valid argument. This is why neutral theory surfaced.
Then what did you mean by this?
âHis claim is that Darwinian process can explain differences up to the genus level.â
It would seem to me that genetic differences between genera can not evolve, according to your description of Beheâs position.
If the alternative splice events are non-functional then they are still near neutral because the functional isoform is still being transcribed and translated. Wouldnât you agree?
It is simply an empirical claim of the limit the Darwinian mechanism.
I donât see empirical evidence of the events being non functional. It looks like lots of activity during embryonic development.
Therefore, the claim is that the differences between the human and chimp genomes could not have evolved since humans and chimps are in different genera, correct?
This is what I think happened.
First, you incorrectly assumed that a change in splice variants meant that 100% of the transcripts were different. What you didnât realize is that there can be multiple versions of mRNA from the same gene, with the most common isoform being the known functional and full length protein.
This first assumption led to the second mistake. You thought that if there is only one gene product and it doesnât have all of the exons then the chances are it will be a deleterious mutation since the new protein will not be functional.
There are also some various other issues that you will need to address. The vast majority of splice variants are less than 1% of total transcripts for a given gene, and most isoforms are thought to be errors in the splicing mechanisms themselves. Also, âdifferencesâ in splicing are often different expression levels of the same splice variants between species.
The first thing you need to support is your claim that most changes in splicing are deleterious. I doubt this will happen, but I am strangely hopeful.
You keep trying to cubby hole the claim but you cannot as it is an empirical claim which is always tentative. You need to challenge it with you own evidence.
This not my claim it is yours.
You need to support your position and not continue to change my claim so that you can support your position with a single exception. You have a problem explaining your hypothesis given the splicing differences. You need empirical support and stop waving your hands.
This is a claim you need to support with evidence during multiple development stages. We see lots of splicing issues in Cancer which is when embryonic pathways are often active.
Ummmm . . . . no. It is up to the person making the claim to support it with evidence. I havenât seen any empirical evidence to back it up. It is just a bare assertion.
How so? What is the problem?
What are the splicing issues, and how do they relate to the genetic differences between humans and chimps?
Until you define what the problem is there is really nothing to address.
So you are claiming that chimps and humans do not share a common ancestor?
https://doi.org/10.1126/science.1230612
The problem is describing the origin of specie specific splicing codes.
You are evading the question.
Therefore, the claim is that the differences between the human and chimp genomes could not have evolved since humans and chimps are in different genera, correct?
The origin is mutations filtered through selection. The differences in alternate splicing is due to the genetic differences between humans and chimps, and those genetic differences are the product of mutation.
So what is the problem with that explanation?
This is not the claim. Have you read Beheâs book?
It has not supported and contradicts the evidence of deleterious splicing mutations.
This is what you said before:
âHis [Beheâs] claim is that Darwinian process can explain differences up to the genus level.â
If evolution can only explain the differences up to the level of genus, doesnât this imply that the differences between genera can not be explained by evolution?
It is supported, as I have shown you many times:
I also donât see the contradiction with the evidence for deleterious splicing mutations. Care to explain?
The claim is around the Darwinian mechanism. The claim is also an empirical claim that makes it tentative.
You support the plane flying 100 ft but your claim is it can fly to Mars. This is why evolution is more ideology than science.
So non-Darwinian mechanisms like genetic drift can explain the differences?
Empirical claims are not tentative, by definition. Empirical claims are direct measurements.
I showed you the evidence that it can fly to Mars. The genetic differences between chimps and humans are consistent with the mechanisms we see producing mutations in humans in real time.
No mechanism so far solves the information paradox.
Empirical claims are interpretations of direct measurements. We know Newtons law of gradation works pretty well on earth but does it work somewhere else in the distant universe.
I respectfully disagree. I donât think you have shown evidence it can fly at all. There are 10k to 50K different splicing variants. How would those get fixed in the population? Drift? Selection?
Then it isnât limited to Darwinian mechanisms only, but applies to all evolutionary mechanisms. Therefore, the use of âDarwinianâ is misleading since Behe is rejecting non-Darwinian mechanisms as well.
No, they arenât. Interpretations are conclusions, not empirical claims.
First, do you agree that these are due to differences in various genetic sequence, be it in the enzymes that transcribe and process RNA, transcriptional regulators that change gene expression, or in the sequences at splicing sites themselves?
Second, do you agree that we observe natural processes causing genetic differences?
Third, do you agree that we see population dynamics fixing mutations?
The reason Behe focuses on Darwinian change is because it is still accepted in the popular interpretation and it has the most directional force.
All this is true but you need enough time and you need to find function.
10K to 50K splicing variants getting fixed in a population is not a trivial problem. 50 million DNA mutations getting fixed in a population is not a trivial problem. Especially mutations that result in specular innovations like language and abstract thought.
Non-Darwinian mechanisms are also accepted in the theory of evolution.
First, you need to show how many of these 10k to 50k variants, if they exist, have function. I see no reason why their mere existence demonstrates that they have function. If 1% of the transcripts for a specific gene are a splice variant and 99% are the standard functional variant, the 1% of splice variants donât need to be functional.
Second, you need to show why any specific number of fixed mutations is a problem for a given time period. From what I have read, the number of fixed mutations between the human and chimp genomes is within the range that evolution would produce.