You admit the possibility that the gene was active and then became de-activated. I would have to look at the genome sequencing of both apes to see if they are in fact two sub-species or not, until then its possible that they are.
When you say "both apes", are you referring to the non-human apes whose genomes were looked at in the study ? If so you should have looked at it before responding. Quoting from the abstract : "Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages.
Please don't tell me you're saying it's possible that chimps, gorillas, gibbons and macaques are sub-species of one another
(If you are
saying that I'd have to ask what definition of "sub-species" you're using, and why humans don't belong to that species too)
Let me tell you about the Duffy gene, Malaria affects humans in which this gene is active. Every now and then a human mutates a "dead gene" somewhere. This dead Duffy gene became simultaneously prolific in two separate populations due to Malaria in each area. Which proves that two separate species or subspecies with similar genomes can have the same mutation becoming prolific in the population if that mutation has similar benefits across both species (eg a disease affecting apes and not humans). Thus it looks like the apes had reduced functionality and the humans retained functionality in that area of the genome.
The odds of the same mutation happening in two different populations is low, but not so low it's impossible (especially when accounting for mutation hot spots) (although it's low enough that I'd be interested in a cite for the claim the Duffy gene became "dead" in the exact same way in two independent populations). But those odds go down dramatically every time you add a mutation, and every time you add a population that purportedly got this mutation independently. Here we're talking about several mutations in four different lineages. The odds are easily in the "negligible" range.
Could you kindly acknowledge this possibility of de-activation rather than activation , you seem to have already acknowledged this in the bolded portion and if the genomes are extremely similar you could be right about these being relatively recent sub-species. I have no problem with that but would have to look at the genome.
Of course I acknowledge this possibility, as you point out I acknowledged it in my response to you, and not only in the bolded portions either (that paragraph about mutations being reversible and us not being able to tell which way they'd gone just from looking at two genes ? That was a direct statement that it could have been a de-activation).
Can we agree that the authors of the paper also
acknowledged this possibility and made substantive arguments for why they dismissed it ?
I call that interesting speculation. Sure it may be possible but never observed. In the meantime its appears impossible for nature to create new active genes. To base the whole theory of the complexity of life on a hypothesis that maybe extra genes can activate seems unscientific to me.
Is it interesting speculation that Pluto orbits the Sun ? Such an orbit has never been observed. For that matter, until last year such an orbit of Neptune had never been observed either. The creation of a new gene hasn't been observed from beginning to end, but "hasn't been observed" and "appears impossible" are two completely different things. Given everything we've agreed upon about how genes work, the creation of new active genes doesn't only appear possible
, it appears to be inevitable
. I understand you disagree with this but I'd like to have an argument as to why this isn't true. "We haven't observed it therefore it's impossible" doesn't work.
I'm also a bit confused by your use of "activate". Maybe you mean "being expressed" ? But we do know of duplicate genes being expressed, the papers we've been discussing are full of examples. And whether a gene is expressed or not depends purely on its nucleotide sequence and the nucleotide sequence of the DNA around it, so changing a gene's expression and changing the nucleotide sequence of a stretch of DNA is the same thing.
The reason I assume this is that we do know that de-activations are favorable. We do not observe a human population with an extra gene in an isolated region showing favorable selective pressure. Yet in the laboratory and in nature we have many instances of favorable mutations involving de-activation of a gene. Thus the one process is more observed than the other process which is completely unobserved. Thus when we come across a section of the genome that is identical in two species yet the one is activated and the other de-activated its not logical to write a paper claiming proof of evolution. Its better to remain neutral , not assuming proof of evolution, and if any assumption is made it should be based on the more proven observed process than the less proven unobserved process. (there is currently a statistical bias towards devolution rather than evolution, some instances of devolution are absolutely proven (dead genes being beneficial), yet no instances of new active protein coding genes are proven to be beneficial to an organism).
Nobody today is writing papers claiming proof of evolution; in biology evolution is considered a proven fact (well, the basics of it at least). Of course creationists don't think it's proven, I'm just saying that's the state of the field. The paper we're talking about certainly didn't claim proof of evolution. They were claiming proof that new genes formed in humans from noncoding DNA. Again, I realize that you consider "new genes forming" and "evolution" to be synonymous, but to biologists "new genes forming" is just one aspect of evolution, and that's what the paper was looking at.
Now you are absolutely right that damaging mutations are much more common than beneficial ones, so that when we look at two almost-identical genes, one functional and the other one not, the most likely scenario is that the non-functional one comes from the functional one. One can't just assume that the functional one came from the non-functional one and is an example of a new gene. But two things : first, this is not what the geneticists who claim to find new genes do
. They have actual arguments
why they think they've found a new gene, and you should address those instead of mischaracterizing their position as "claiming proof of evolution" just because they "came across a section of the genome that is identical in two species yet the one is activated and the other de-activated".
And second, while it is true it is less likely
for a mutation to turn a noncoding stretch of DNA into a gene rather than the opposite, your argument is much stronger than that : you are saying it's impossible
. That argument is what I would like you to justify.
You seem to make a good point here, but the reality is that the neutral gene cannot change and activate beneficially.
Why not ? Please give arguments for this, don't just assert it. Or should I say, given what comes next, please give arguments that are based in how genes actually work.
To put this into simplistic terms, imagine a secret code that is designed to produce a foot. Duplicate it. No problem, the duplication is inactive. Activate it. Now you have three feet with two legs. BIG problem. The same applies to subtle things like heart speed, it must go with the right size of body, correct heart muscles, veins that can handle blood flow. I don't know much about biology but can you see the problems when you duplicate an active gene without redesigning the entire organism at the same time? Even if you mutate the active gene, much of that gene will still retain the original function and you would have a problem with the activated duplicate duplicating a lot of the functions of the original. Duplicates are good as "backup systems", not as active genes.
I'm sorry but this isn't how genes work at all. For one thing, there is no reason the duplication would be "inactive" to start with. The reason genes get "deactivated" is if there is a mutation to some of the surrounding DNA that keeps them from being expressed, or a mutation to their nucleotide sequence that means the protein they code for doesn't work. If a duplicated gene gets duplicated into a part of the genome where it will be expressed, and if its nucleotide sequence isn't altered in a way that makes the protein non-functional, it will be as "active" as the original gene was. (epistatic interactions put a wrinkle on that but I think the principle is there)
Second, genes don't code for feet, or heart speed, or body size, or heart muscles, or veins. They code for proteins. When a gene is duplicated and continues to be expressed it can have results such as twice the normal amount of proteins being produced, or more or less than twice depending on the interactions with other genes, or those proteins being produced in a different part of the body, or at a different point during development, so on so forth. Such differences in proteins can be harmful, but they can also be beneficial. More often they're neutral.
There are genes that can be said to "code for" macroscopic structures like limbs or organs, but those are the regulatory genes you're ignoring. And even there duplicating them won't always have the same dramatic consequences - it really depends on the gene and where they got duplicated to.
I believe the balance of evidence at the moment is pointing to the sudden appearance of already advanced life-forms. (the evidence being the difficulty to create new good active genes).
Up to now I thought you were saying it was impossible for nature to create new active genes, is this a change in position, a different way of saying the same thing, or did I misinterpret your original position ? If I did I apologize. I would still like to know how
difficult you think it is to create new genes. Like, in a population of 1000 individuals how many generations would you expect to pass before you saw a single new gene ?
Thus no new genes are needed, You seem to think that evolving should occur anyway. Its absolutely unnecessary if the design was good in the first place. Yes the number of allele combinations is multiple trillions times by multiple trillions so the ability for each creature to adapt to its environment is already there, but you do not need more than that with well designed creatures.
I'm not talking about "need" here. I'm talking about what statistics say will happen given what we know of how mutations work. Now you do bring up another valid barrier to new genes arising : if every organism were so perfectly adapted to their environment already that absolutely no mutation could be beneficial then beneficial new genes couldn't arise. But given we've already agreed that beneficial mutations can happen I'm not sure why you bring it up.
Again were those HAR regions designed or created like that ? Its hard to tell when we just know its there already. Yes there's other aspects important to evolution but I still want to focus on the necessary process of adding extra good protein-coding genes so I do feel that's a distraction.
Well of course those HAR regions, like every single other thing in the Universe, could have been "designed and created like that" by an omnipotent creator. So could any gene that looks as if it's a result of duplication and mutation, so I'm not sure why it's a distraction. I have no issue with people who think God created life and made it look as if it had evolved; it's not scientifically testable but people's personal beliefs don't have to be scientifically testable if they don't want them to be. That said it's true I keep forgetting that you draw a sharp distinction between new genes formed from existing genetic material, and new genetic material, and HAR are an example of the former. Sorry about that.
I deleted one post when I realised I was replying to your same post twice, maybe that's it. If you describe what I said we could talk about it, but I think we have enough to go on, and I like to keep narrowing the conversation to a conclusion rather than increasing discussion topics, which can get impossible to deal with.
Yes that was it; I remember being rather confused by the response so I'm glad you ended up editing it ^^
EDIT : Because it seems you edited your post after I started this response, so I'll respond to the added bits here :
2) They both have the same disabler (indels) which definitely points to subsequent non-coding, they wouldn't call the disabler an indel if it was already there.
3) They could both have independently gained non-coding regions in the same place because of the same environmental pressures on both types of apes as can be seen in the human Duffy gene.
2) As I said, mutation is a completely reversible process. Whether a mutation is "disabling" or "enabling" is really an assumption of which version of the gene came first. I agree it's confusing that they'd refer to "disabling" mutations in the primate genomes; I figure it must be their habit to refer to non-functional bits of DNA in reference to the functional genes they resemble regardless of which came first. It is crystal clear however that they think the non-coding primate DNA bits came first; one can disagree with their conclusion but you can't really use their confusing language to suggest they don't really think what they wrote a whole paper to say...
3) The issue isn't that the regions are non-coding, it's that they're non-coding in the exact same way. Functional, coding regions we might expect to be similar because they're constrained by their function. Not so with non-coding regions. When disabling a gene is selected for (as you say is the case with the Duffy gene), then any mutation that disables it works. There is no reason to expect it to be disabled the exact same way in four different populations.
Down's syndrome produces extra proteins, i assumed because the duplicates are active. Either way, I suppose the syndrome points to additional activity to the norm being destructive. I feel this is generally observable.
(this is probably a bit I missed more than that you added, but anyway) : additional activity to the norm can be destructive, especially when the difference is as huge as what you get with Down's syndrome, but it isn't always. And I am still confused by your terminology : if having a duplicate that's expressed counts as a new gene, then again we've got tons of non-harmful cases of that if only in plants.