Unfortunately I can’t read the whole paper, but I’m curious about your thoughts on this.
If humans don’t have regulatory elements that animals do - regulatory elements which turn off genes, does that mean that the human genome was first in God’s will? Interesting thought.
If we look at this from a materialistic standpoint, some information that made us human was already existent, and then those regulatory elements weren’t selected against for how many millions of years? But they were only selected against in the human lineage in a much shorter time frame? I wish I had more info from the paper. Let me know if I’m also reasoning anything wrongly there.
If God made a will, does that mean that he’s dead? More importantly, have you considered the possibility that other animals also have deletions in various sequences that are conserved too? Consider the possibility that this is not a way that humans are unique except in the narrow consideration of the particular sequences, out of all the myriad sequences in the genome. Note that the average deletion is only about 3 bases, which doesn’t eliminate the conserved sequence, just makes it a little shorter.
I’m confused how you come to this conclusion. There are 510 identified hCONDELs (human-specific deletions in conserved regions), and there are also 350 identified mCONDELs (mouse-specific CONDELs) and 344 identified cCONDELs (chimpanzee-specific CONDELs) mentioned in that paper. Does that mean that mice and chimpanzees were tied for first-place with humans in God’s will? How do CONDELs indicate that a species is first in God’s will, anyway?
Also, seeing as mCONDELs and cCONDELs are mentioned right on the first page of that paper, I have to ask, did you read the paper before posting here?
Perhaps instead of mentioning I wasn’t able to read the whole paper (which are the first words of my post), I should have been clearer that I don’t have access to anything but the structured abstract and a figure, neither of which mentions anything besides hCONDELs. The figure says they identified 10,032, so I don’t know why the discrepancy in numbers you’re cited. I’m a little annoyed you accused me of not reading the paper though, when I literally led with that statement.
I’ll see if anyone has any thoughts before I comment more. I am very curious how selection would work in this case, or in any case where an earlier branch of the tree would repress a gene that later branches express. It makes sense to me if one was designed first, or they all were designed as a set, but I can’t fathom how randomness and natural selection would arrive there. Just asking in case I just don’t get it.
I also am curious if this paper validates some of the ways Tomkins counted chimp-human differences since these small deletions seem to have functional differences. I’d have to find his lay audience articles though because one of the papers I found and read last night was above my understanding.
I’ll note that the complete paper is paywalled. However even the abstract does not seem very friendly to your idea,
That seems a massive non-sequitur.
A massive non-sequitur based on a misreading of the abstract, at that. The paper doesn’t claim that the regulatory elements are absent in humans. It’s about regulatory functions affected by deletions - which only remove part of the regulatory element. So the regulatory elements are still at least partially present -about half of those tested have enhanced function which is hardly possible if the entire element was deleted.
You mean regulatory elements that function by shutting off expression, transcriptional silencers, repressors? Those are things that “turn off” genes. Humans have transcriptional silencers. Lots of them. Many of them silence retrotransposon-derived sequences to keep them from messing stuff up(which is one among many ways we know those silenced regions are mostly retrovirus-derived junk DNA).
I was going to reply in the same way that others already had. Many genomic analyses will concentrate on the human genome, as that garners greater interest (and funding). But it is quite reasonable to expect that all species will have similar small changes in regulatory DNA when compared to related species.
That issue of Science is of interest, though. I suspect it will cover the interesting story of how placental mammals evolved into different taxons as northern land masses separated during the late Mesozoic. This story includes patterns of divergent evolution within a land area, but also convergent evolution between separate lands. It’s rather like the well known story of how placental mammals and marsupial mammals evolved.
In their study, the Yale team found that some genetic sequences found in the genomes of most other mammal species, from mice to whales, vanished in humans. But rather than disrupt human biology, they say, some of these deletions created new genetic encodings that eliminated elements that would normally turn genes off.
The deletion of this genetic information, Reilly said, had an effect that was the equivalent of removing three characters—“n’t”—from the word “isn’t” to create a new word, “is.”
“[Such deletions] can tweak the meaning of the instructions of how to make a human slightly, helping explain our bigger brains and complex cognition,” he said.
Ok, so if some of those have enhanced function, what I am suggesting is that if you compare mammals to humans, instead of comparing humans to mammals, it appears other mammals have additional letters to repress function that the human genome expresses.
I don’t have a very clear understanding of the biological processes going on here. Yes, sure humans have a lot of regulatory elements that turn off genes. Again, I just looked at this paper as saying other mammals have elements that turn down or turn off genes they share with humans.
I’m just trying to understand how this programmer works - as my perspective is that genomes are designed. To me it looks like there’s functions throughout that can be turned off or on or turned down or up when you compare all mammals and the genes they share.
So maybe the programmer designed the whole set together perhaps, or had one as a reference before designing the set. This was more efficient than creating a program with all functions specific to each kind when some desired functions were broadly similar.
If genomes aren’t designed, then someone should be able to provide a reason why selection is a superior explanation here. Anyone?
A random deletion in a repressor that used to silence expression of a gene, results in it no longer silencing the genes expression, and that change in expression has a positive effect on fitness in the environment now occupied by the species.
Just one scenario that is simple enough to think up, consider where expression of a gene coding for an enzyme that breaks down some food source that used to be scarce would previously be costly since it rarely had any use, since the food was almost never available.
But now instead expression of the gene is beneficial because the food source has become an abundant and staple part of the diet which the organism is continuously digesting.
That’s how, just as a hypothetical example, a change from silencing to expression can be beneficial.
The random deletion in the silencer took away it’s silencing effect, and the gene is now permanently turned on, and the environment the species lives in has changed such that the genes silencing was previously beneficial, but is now deleterious, and it’s expression used to be deleterious, but is now beneficial.
True up to a point. But they turn them down or off at some times or in some environments, not all the time. In humans, those genes get turned down or off somewhat less at some other times or in some other environments. It’s not like the genes were just waiting around to be expressed in humans. Useless genes turn into pseudogenes.
Also remember that these sorts of deletions don’t just happen in humans; they happen in all species. We are by no means special in that respect. We have some particular set of deletions, and other species have different particular sets of deletions.
I think you jumped to conclusions since the material you quote doesn’t say that the entire regulatory sequence was removed. Indeed, read carefully it agrees that only parts were lost.
But what makes that the right way to do the comparison? In my thinking - without assuming common descent - the only difference which would tell would be a partial deletion that destroyed the regulatory function. That would fit better with the regulatory function existing first. And there may be examples of that in this data set, although the abstract doesn’t say, (Of course, since common descent is well supported it assuming it would be perfectly proper in a scientific study).
That’s a good example, thanks. I really wish I had all the details of the paper.
The problem I see then is that because these are conserved sequences, they are selected for again and again because it’s so useful for whatever gene to be repressed in mammals (yet the gene wasn’t deleted). In contrast, these conserved sequences are selected against when it comes to humans, and some affect neuronal activity. Why should natural selection work strongly against that?
And either of these options predict what feature of any genome? Designed the whole set together leads us to expect what in particular? Having one as a reference and then designing a set based on that produces what effect?
I don’t see you actually explain anything. No fact of the matter with respect to any genome is explained in any way.
I doubt God as the purported creator of the entire universe is much concerned with efficiency of any sort. There is no resource scarcity possible, be that limited time, energy, matter or what have you, that could ever constrain what he could possibly create.
The concerns you are imagining here only make sense to someone who is limited in some way, like human biochemists who have limited knowledge, time, patience, materials etc.
The advantage evolutionary explanations have is that they actually explain stuff. And they can be observed and tested. Mutations have known and observed biochemical causes, they demonstrably have fitness effects. Some times historical evolutionary changes can even be inferred from a phylogenetic tree, re-created in the laboratory, and tested for their effects. In a process known as ancestral sequence reconstruction.
Once again, the gene wasn’t deleted because it wasn’t repressed all the time. It was expressed in some tissues at some times. In humans, it’s possibly expressed in more tissues, or at other times, or perhaps just more often. Those are not pseudogenes.
Right. But mutations don’t occur just because they might be beneficial if they did. They’re essentially random. Deletions come in different sizes, some small some large, and everything in between, distributed throughout the genome.
Some gene being repressed because it’s activity is deleterious doesn’t mean the gene being repressed is guaranteed to get deleted wholesale (or incrementally), dependent on time scale of course. And that time scale factor is also relevant. If large specific deletions are very rare, but smaller ones are more frequent but it would take many consecutive ones to entirely delete a gene, how long would it take, on average, for some specific locus to get entirely deleted? 1, 5, 25, 50 million years? An answer to that question will explain why it isn’t mysterious some loci that are deleterious when expressed nevertheless manage to stick around. Another factor is that some of these loci are parts of active transposons, so even though some do get deleted, others are continously copied and inserted, then suppressed, so they have very tiny fitness costs and can propagate selfishly in the genome.
In a way this is actually an argument for the blindness evolution. We can imagine a circumstance that would more benefit the organism than an active suppressor protein: the locus being suppressed getting entirely deleted. But that’s not the mutation that happened.
Instead a mutation happened that was good enough to be beneficial, but it’s not the best one possible. And hey that turned out to actually be an advantage here, because the locus being suppressed later turned out to be beneficial when expressed, so a small deletion in the suppressor(removing it’s ability to suppress expression) could be favored instead.
They affect neuronal activity in a way that produces deleterious behavior? I don’t see how this is a question. Natural selection works against it if it has a negative effect on survival and reproduction. Presumably there is forms of neuronal activity that does that. I’m going to conjecture that in most natural circumstances, neuronal activity associated with thinking you can fist-fight a flock of hungry lions, or abstaining from procreation, is among those less than selectively advantageous types of neuronal activity.
I will think about the questions, but I’d ask you what modern evolutionary theory predicts that unique to it? It seems biologists continue to be surprised.
IMO, you’re not thinking about this correctly. God’s mind is unlimited, but creation itself will always be limited no matter how big it was initially created to be. It was created with order to follow certain laws because God is good. So yes, we would expect God to be concerned with efficiency as much as we would - sometimes efficiency can be secondary to aesthetics, etc. I’m guessing there are trillions of biological processes going on in my body at any second - seems rather efficient to me.
Exactly what here do I disagree with exactly? Design proponents also agree with change over time.
Which gene are you referring to here? “It”? The LOXL2 gene mentioned in the paper?
I’m referring to the genes you were referring to. The reason these genes aren’t deleted is that they are expressed, and have functions, in all the animals that have them. They’re just expressed a little more often, in some tissues at some times, in humans. Genes are expressed (technically this term applies to the proteins, not the genes), or not, in response to signals, such as transcription factors, that change in an animal depending on place, time, and environment.
Then your hypothesis is falsified by mountains of data.
Take, for example, the fact that start codons place the same amino acid residue at the beginning of every protein, and contrast that with the fact that a huge proportion of functional proteins have had that residue removed.
A far more efficient strategy would be to have the start codon not specify an amino acid, as the stop codons do.
Evolution explains this disparity easily, while design does not.
