Chimps and humans: How similar are we really?

Loudmouth

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And my point is that DNA analysis (might) match form and function observations
not to confirm "relationships", but to confirm form and function similarities.

Your point is wrong since you can have very different DNA sequences for the same function.
 
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Loudmouth

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All birds have beaks, or bills. Ducks and geese have broad, flat beaks for straining food out of the water.

The platypus does not have a bird beak. They are very very different.

Platypus
sp3026-70d22b62.jpg


Duck
category2_order_28_large.jpg


That is not a shared feature. The lower jaw is even better since the bird's lower jaw is made up of multiple bones like other birds but the platypus lower jaw is made up of a single bone just like other mammals.

All birds have wings, as do insects, although not all birds fly.
41GhmGzpbCL._SL500_AC_SS350_.jpg
bat.jpg

Wing is the name of a function, not an anatomical structure. The wings of birds, insects, and bats are all different. Bat wings are not bird wings.
 
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PsychoSarah

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Both creatures were made by Lord God/Jesus as temporary creatures which are called creeping things in Scripture.

Gen 6:20 Of fowls after their kind, and of cattle after their kind, of every creeping thing of the earth after his kind, two of every sort shall come unto thee, to keep them alive.

Their kinds are the kinds which God created from water on the 5th Day. Gen 1:21
His kinds are the kinds which Lord God made temporarily such as mankind. Gen 2:7 In order to have Humans who live forever, mankind MUST be born again Spiritually by God the Trinity. Gen 1:26 Gen 5:1-2 AND John 14:16 God Bless you
-_- then I guess you'd call bacteria "creeping things" too. That'd make the "kind" of "creeping things" so broad as to be useless for descriptive purposes. It doesn't even distinguish by cell type.
 
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Aman777

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-_- then I guess you'd call bacteria "creeping things" too. That'd make the "kind" of "creeping things" so broad as to be useless for descriptive purposes. It doesn't even distinguish by cell type.

Amen, but here's why creeping things are different. They were made by Jesus, which means they are subject to death. From dust they are made and from dust they shall return UNLESS they are born again Spiritually by the invisible God. Amen?
 
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PsychoSarah

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Amen, but here's why creeping things are different. They were made by Jesus, which means they are subject to death. From dust they are made and from dust they shall return UNLESS they are born again Spiritually by the invisible God. Amen?
Are you unaware that there are organisms which are functionally immortal and thus, barring being consumed or killed by disease, they don't die? For example, there is a species of jellyfish that cycles between being an adult and returning to it's equivalent of a child state. The Nepenthes I grow have no correlation between their age and death and the small species that don't vine could live indefinitely, as they will never grow to the point of being structurally unstable. Well, those, and ones grown in cultivation that are trimmed periodically.
 
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Aman777

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Are you unaware that there are organisms which are functionally immortal and thus, barring being consumed or killed by disease, they don't die? For example, there is a species of jellyfish that cycles between being an adult and returning to it's equivalent of a child state. The Nepenthes I grow have no correlation between their age and death and the small species that don't vine could live indefinitely, as they will never grow to the point of being structurally unstable. Well, those, and ones grown in cultivation that are trimmed periodically.

No flesh is functionally immortal since everything Jesus made (His kinds) are subject to death UNTIL death is destroyed at the end of the present 6th Day. Then, those who have put on immortality, will live longer than Nepenthes. God Bless you

1Co 15:26 The last enemy that shall be destroyed is death.
 
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PsychoSarah

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No flesh is functionally immortal since everything Jesus made (His kinds) are subject to death UNTIL death is destroyed at the end of the present 6th Day. Then, those who have put on immortality, will live longer than Nepenthes. God Bless you

1Co 15:26 The last enemy that shall be destroyed is death.
-_- the jellyfish is demonstrably functionally immortal. Functional immortality means that an organism's cells do not age after a point, or that the organism has a process by which to rejuvenate cells such that aging is reversed periodically. Anything that is functionally immortal will not die of old age.
 
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mark kennedy

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-_- thanks for lumping in autistic people like myself with schizophrenics and people with bipolar disorder. None of those disorders actually limit reproduction much. Heck, all three require currently unknown environmental cues to even afflict a person. For all you know, you have a genetic predisposition to one or all three of those disorders, and you just never ended up with them by lucking out on your environment.

Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.

That's not true, in a previous debate, I listed off ones by official label. Others have done so in this very thread. I shouldn't have to keep looking up the official labels every time I bring up these mutations.

You seem to have missed the point that mutations in brain related genes have deleterious effects.

1. I'm too distracted by you ignoring the examples of beneficial brain gene mutations to want to give much thought to your continued, shallow, emotional appeal of how ridiculous you think it is for mutations to be the reason why human brains are larger than those of other apes.

But you didn't do that, you keep referring to arguments you never made. Now there was some discussion of Hox genes which hardly account for the massive overhaul of brain related genes 2 mya.

2. I don't view this as "a critical point". Brains are like any other organ, you might as well be incredulous about the evolution of lizard bladders. You've failed consistently to properly defend your position that mutation can't contribute positively to human intelligence, especially when it comes to the positive brain mutations you keep deciding to ignore.

The obvious fact here is we are not talking about a bladder. The human brain is developed by a large number of highly conserved genes. The effects of mutations on the human brain from mutations are always deleterious, when they actually have an effect.

3. I'm not going to pretend that other people haven't given you official labels for positive brain mutations in humans, only for you to ignore them. You have to demonstrate that it is even worth my time to debate with you any more, by actually addressing the claimed positive mutations. You don't have to treat them as valid, I don't care how much denial you want to be in, just acknowledge people have given you examples of these positive mutations and you disagree with their claims or the studies that show them. Ignoring these points is just insulting to the people debating with you.

There have been no such proofs, arguments or even a serious suggestion. It's called begging the question of proof.
 
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PsychoSarah

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Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.
Don't pretend that the mutations being present in and of themselves doesn't mean a person will have the disorder is irrelevant. It is extremely relevant; why would it matter if there are more detrimental mutations than benign ones if the detrimental effect doesn't consistently happen?


You seem to have missed the point that mutations in brain related genes have deleterious effects.
And you keep ignoring that brain related mutations don't always result in negative effects. It's not like we'd name the conditions that result from the benign ones. We just say some people are better at math, etc.



But you didn't do that, you keep referring to arguments you never made. Now there was some discussion of Hox genes which hardly account for the massive overhaul of brain related genes 2 mya.
-_- the brain related genes we were discussion aren't HOX genes. Not all brain related genes are HOX genes, in fact, nearly all HOX genes are genes that guide the differentiation of organ tissues and body anatomy position. Where the brain goes, not how big it gets.



The obvious fact here is we are not talking about a bladder. The human brain is developed by a large number of highly conserved genes.
I literally Google searched this last time it came up and found out that brain related genes are some of the most mutation prone in our species. What source is telling you the opposite?

The effects of mutations on the human brain from mutations are always deleterious, when they actually have an effect.
https://www.scientificamerican.com/article/genetic-mutation-sleep-less/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals
Sources on the DEC2 gene mutation that, when present in humans, reduces the length of time needed to sleep. It has an effect, and it isn't detrimental or resulting in the loss of a function. This better be the last time I have to mention this.

Note that the purpose of the original study that found the mutation and its effect was to find genes that regulated sleep in humans. They noticed that all people that required less sleep to function normally had an unusual sequence, and were able to determine the function of the gene that way.


There have been no such proofs, arguments or even a serious suggestion. It's called begging the question of proof.
The DEC2 gene mutation has been demonstrated to exist, and its effect in humans has been known since 2009.
 
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mark kennedy

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Don't pretend that the mutations being present in and of themselves doesn't mean a person will have the disorder is irrelevant. It is extremely relevant; why would it matter if there are more detrimental mutations than benign ones if the detrimental effect doesn't consistently happen?

Don't pretend that's what we are talking about because you know better. We are talking about an effective cause for the three fold expansion of the human brain, and you don't have a single example of a beneficial effect from a mutation in a brain related gene.


And you keep ignoring that brain related mutations don't always result in negative effects. It's not like we'd name the conditions that result from the benign ones. We just say some people are better at math, etc.

Never said they did although I've never seen a real example. The math tells us that the overwhelming, if not exclusive, effect of genetic mutations on brain related genes is deleterious. Examples to the contrary are nonexistent.


-_- the brain related genes we were discussion aren't HOX genes. Not all brain related genes are HOX genes, in fact, nearly all HOX genes are genes that guide the differentiation of organ tissues and body anatomy position. Where the brain goes, not how big it gets.

A cute statement, not related to adaptive evolution.

I literally Google searched this last time it came up and found out that brain related genes are some of the most mutation prone in our species. What source is telling you the opposite?


https://www.scientificamerican.com/article/genetic-mutation-sleep-less/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals
Sources on the DEC2 gene mutation that, when present in humans, reduces the length of time needed to sleep. It has an effect, and it isn't detrimental or resulting in the loss of a function. This better be the last time I have to mention this.

Well I do hope this is the last time you bring it up because the short term effects of brain related genes in mice doesn't interest me much.

Note that the purpose of the original study that found the mutation and its effect was to find genes that regulated sleep in humans. They noticed that all people that required less sleep to function normally had an unusual sequence, and were able to determine the function of the gene that way.

The DEC2 gene mutation has been demonstrated to exist, and its effect in humans has been known since 2009.

A mutation that helps you sleep isn't exactly a viable means for 60 de novo genes. The example is at best anecdotal.
 
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tas8831

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And my point is that DNA analysis will match form and function observations
not to confirm "relationships", but to confirm form and function similarities.

So dolphin and shark DNA should be pretty similar, huh?
 
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tas8831

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pshun2404 - really hoping you will address this instead of avoiding it.
pshun2404:
Look at this alleged “same gene” across species...an ALLEGED shared gene...

Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long

Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.

The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.

Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!
Had you considered the possibility that those 'same genes' were not sequenced to the same extent?

When I was in graduate school, we we comparing 2 introns from a gene across several species. We used the human gene - the entire coding region, plus introns, plus 3' and 5' flanking regions - as a reference. For some taxa, our genomic DNA samples were old and we had limited success in sequencing the introns. In others, we had no problems at all. The primers we used to generate PCR fragments were in exons because they were fairly well conserved, and so for some taxa we had not only the introns, but parts of exons as well. several taxa had extensive repetitions in their introns, making one, for instance, nearly 1kb larger than all of the others.
By your implicit logic, we should have concluded that these sequences were not from the SAME GENE, despite the fact that we have amplified fragments using identical primers (30+ years of reading on these subjects should be sufficient for your understanding of the above).

I suggest that the human gene you refer to includes all intronic sequence and flanking regions, whereas the others are limited to smaller regions (e.g., without the flanks, or just mRNA).

In fact, I am willing to bet on it.

What say you?
 
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Tanj

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You seem to have missed the point that mutations in brain related genes have deleterious effects.

Same way you missed the 16 mutations in HAR1A that I posted that are not deleterious. Your constant repetition of the same proven falsehood over and over doesn't make it any more true.
 
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PsychoSarah

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Those are examples of genetic mutations having a deleterious effect on the brain, nothing more.
I don't know why you feel the need to keep mentioning that there are mutations that result in detrimental effects on the brain. There are mutations for every organ that will mess it up to various extents.


You seem to have missed the point that mutations in brain related genes have deleterious effects.
BUT NOT EXCLUSIVELY. ALL MUTATIONS IN BRAIN RELATED GENES DO NOT RESULT IN DETRIMENTAL EFFECTS. So, what is the point of bringing this up all the time? I know plenty of mutations result in horrific mental defects. But not all of them do, and some are measurably benign.


But you didn't do that, you keep referring to arguments you never made. Now there was some discussion of Hox genes which hardly account for the massive overhaul of brain related genes 2 mya.
I will hunt down the thread so help me. Nothing irks me more than being accused of being a liar. It wasn't even that long ago, the thread is within the first two pages of the subforum.


The obvious fact here is we are not talking about a bladder. The human brain is developed by a large number of highly conserved genes.
Which are not conserved in humans at all. Before, you specified the gene area for this, making it very easy to look up the fact that it was one of the most frequently mutating gene regions in humans.

The effects of mutations on the human brain from mutations are always deleterious, when they actually have an effect.
So you are just going to ignore the multiple benign brain mutation examples people have given you, as well as the specific one I PROVIDED SOURCES FOR. Threads aren't fresh starts every time, you can't act as if I haven't provided sources within a currently active thread you are participating in. You can't pretend we haven't conversed on this matter before.


There have been no such proofs, arguments or even a serious suggestion. It's called begging the question of proof.
Genetic basis of human brain evolution overall about the genetics of human evolution, including the brain.

https://www.scientificamerican.com/article/garbled-dna-might-be-good-for-you/ how widespread significant mutations in somatic cells are in healthy people. 30% or more of your liver cells have an extra chromosome or are missing one, for example.

https://www.nih.gov/news-events/nih-research-matters/gene-regulates-sleep-length DEC2 genetic mutation that allows for less sleep... again. The specific label for the mutant version of the gene being hDEC2. I will not stop mentioning this until you listen.
 
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tas8831

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There is a lot here so let me start slow....

Ok, great! Thrill me with your acumen!
Any study of Phylogenetics (and in our training to understand it) we see two aspects of it, one being theoretical and the other being empirical. And the opinions for or against are extant dependent on the definition of terms. This means that even though most may agree, it is largely opinion not established fact.

You started out OK, then went pure Duane Gish. Phylogenetics is "Largely opinion" you say?

I suggest maybe reading Felsenstein's "Inferring Phylogenies" or Nei and Kumar's "Molecular Evolution and Phylogenetics".

For example, we hear the term “relationship” being repeated over and over but when we see what we see (similarities in genetic materials, arrangement, and purpose) the question is “What does this mean?” It can mean related as in somehow similar (size, place, function, etc.) OR does it actually show we are related in the sense of demonstrating lineage (that one comes from the other)? well therein lays the dilemma that breeds discussion and debate.

What it ACTUALLY shows is some semblance of similarity, and this not nearly as exact as the rhetoric would like you to be convinced of.

Speaking of rhetoric...

You do realize - given your claims of decades of reading and work in the relevant sciences - that molecular phylogenetics methods are TESTED? Their outputs are not 'opinions'. Due to the nature of molecular data there are certainly confounding phenomena that can, depending on the type and amount of data being used, produce inconsistent outputs and the like. But that no more invalidates molecular phylogenies than does the fact that there are Old Earth Creationists and Young earth Creationists and this invalidates the veracity of Scripture (there are other things than can do that).

If you really look at the data (void the narrative attached that explains the data according to the already accepted pre-conceived notion) we suddenly realize that the shoe does not fit the foot....

Such projection is rarely seen in the public at large, but it is part of the anti-evolutionist's tool kit.
Look at this alleged “same gene” across species...an ALLEGED shared gene...

Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long

Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.

The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.

Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!

This is the crux of my 'challenge' that you eventually addressed here, but as is your usual fashion, you wrote much more than was needed to simply avoid actually addressing the issue.

The issue I brought up is that you seem to focus on the length of the sequences. I pointed out that it is very common to have differing lengths of sequence for the 'same gene' due to areas of interest, reference sequences, sequencing difficulties, etc., and wondered if you had or would look into that possibility rather than attributing it all to some nefarious conspiracy.

Your response was largely irrelevant, but the bottom line, in my estimation, was that yes - you focused solely on the length of the sequences, which, due to my knowledge of the techniques involved and the impetus for generating sequence data in the first place, was superficial at best. As seen here:

Now as fit as the hypothesis based explanation appears, the actual data shows us they actually are nothing alike...they are different in size AND FUNCTION...yet billed as “commonly shared” in the rhetoric.

Seems that your decades of reading would have informed you that genes often acquire different functions (e.g., genes important during development often play rather mundane roles later on) and that genes can be copied/modified and end up performing other functions.


But I suppose all that amassed knowledge is all just 'speculation' and opinion, too, right?
Well since what I am telling you is true, how did they convince so many?

Half-true, at best.

I do enjoy the substantial amount of projection that ensues:

This process of convincing the masses of the speculative for a definite motive (to prove their theory) requires consistent:

a) Interpretation of all data (even that which could be considered contrary to that theory) though the accepted model as opposed to allowing the raw data shape and remake the model (which is good science and true critical thought)


b) Repetition over and over...early Psychologist William James discovered this characteristic of people...that if they hear, or have had modelled before them, something not really true, over and over and over, they come to believe it as if it is true. Goebbels, capitalized on this insight in the 1930’s in Germany and applying it to politics h says “If you tell a lie big enough and keep repeating it, people will eventually come to believe it. The lie can be maintained only for such time as the State can shield the people from the political, economic and/or military consequences of the lie. It thus becomes vitally important for the State to use all of its powers to repress dissent, for the truth is the mortal enemy of the lie, and thus by extension, the truth is the greatest enemy of the State.” The same is true in this matter. Those aspects which are merely opinion about the data are repeated over and over as if they are fact and the masses swallow it whole with no actual discernment taking place.


c) Appeal to Authority...the above is reinforced by this. In addition to the repetition of the COULD BE/MIGHT BE over and over (which brainwashes) when you get a bunch of alleged authorities saying “Yes It is true”....simply because of their sheepskin people say “Well it must be true after all they know”. Really? NOT!


d) And then finally through c) consensus follows (the argumentum ad populum)....which basically is that “if everyone is saying it is true then it must be true” but if history (even the history of science) has taught us one thing it is that just because a bunch believe it does not make it so.

You just described creationism to a T.


So Phylogenetics, which says different groups and in some sense ALL living organisms share genes, this is correct (but not nearly as many as they claim...see my above “shared gene” example)...but what this means is where we enter the twilight zone of opinion and interpretation. So let me ask...

If you were NOT ALREADY CONVINCED of the theory, and you were to just view the “shared gene” data above for the first time...(please be honest here) objectively, as a scientist, would you really come to some conclusion of lineage? They do not progress and they are not in any way the same (not actually)!
Actually, if I had only the shallow, cherry-picked information you provided, I might be skeptical.

Alas, when I chose to work in phylogenetics lab in grad school, I was exposed to REAMS of data, not just a couple of cherry-picked 'what-do-you-think-of-THIS!!!' poorly described examples.
When one looks at the totality of available evidence (or even a chunk of it), looks at the actual large-scale patterns as opposed to a couple of anomalies, it becomes not just intuitively correct, but empirically supported conclusion.
 
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tas8831

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It is an amazing thing.


I found it difficult, using the normal sources (NCBI), to confirm the numbers supplied below (e.g., 87,092 bases for HDLBP). So, I just googled "Human Gene HDLBP" as written ...

Look at this alleged “same gene” across species...an ALLEGED shared gene...

Human Gene HDLBP (uc002wba.1) a 110-kD protein that specifically binds HDL molecules, which functions in the removal of cellular cholesteral...it is a section 87,092 base pairs long

Rat Gene Hdlbp (NM_172039) which is only 68, 238 base pairs long performs a similar function but apparently not identically.

The allegedly the “SAME GENE” in Yeast, S. cerevisiae Gene SCP160 (YJL080C) functions differently and is primary to cell division, and only has 3,669 base pairs.

Finally, the alleged “SAME GENE” in D. Melongaster, Gene Dp1 (CG5170-RB). Having 9119 base pairs (3 times that of Yeast) seems to do nothing!

... and darned if I did not find this:


For example, Human Gene HDLBP (uc002wba.1) is a "High density lipoprotein-binding protein, also known as vigilin, is a 110-kD protein that specifically binds HDL molecules and may function in the removal of excess cellular cholesterol." It is 87092 base pairs long.

In other species it is:
(Rat) Rat Gene Hdlbp (NM_172039) - 68238 base pairs - also performs a similiar function.
(Fly) D. melanogaster Gene Dp1 (CG5170-RB) - 9119 base pairs - not sure what it does
(Roundworm) C. elegans Gene C08H9.2 (C08H9.2) - 3900 base pairs - not sure what it does
(Yeast) S. cerevisiae Gene SCP160 (YJL080C) - 3669 - where it is thought to be used in cell division​

at Yahoo Answers from 10 years ago.

The link provided then is dead, which may be why I cannot verify the numbers.

Isn't that an amazing un-cited coincidence????
 
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mark kennedy

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I don't know why you feel the need to keep mentioning that there are mutations that result in detrimental effects on the brain. There are mutations for every organ that will mess it up to various extents.

Because you think they are a vehicle for adaptive evolution, I know better.

BUT NOT EXCLUSIVELY. ALL MUTATIONS IN BRAIN RELATED GENES DO NOT RESULT IN DETRIMENTAL EFFECTS. So, what is the point of bringing this up all the time? I know plenty of mutations result in horrific mental defects. But not all of them do, and some are measurably benign.

All I'm finding is tumors, cysts, cancer and an array of neurological disorders. Now if you want to assume neutral or nearly neutral effects I suppose that's your prerogative but they are not going to result in adaptive evolution.

I will hunt down the thread so help me. Nothing irks me more than being accused of being a liar. It wasn't even that long ago, the thread is within the first two pages of the subforum.

I don't think your lying, I think you've been taken in by this Darwinian mutations plus natural selection equals adaptive evolution. It never stands up to close scrutiny.

Which are not conserved in humans at all. Before, you specified the gene area for this, making it very easy to look up the fact that it was one of the most frequently mutating gene regions in humans.


So you are just going to ignore the multiple benign brain mutation examples people have given you, as well as the specific one I PROVIDED SOURCES FOR. Threads aren't fresh starts every time, you can't act as if I haven't provided sources within a currently active thread you are participating in. You can't pretend we haven't conversed on this matter before.

I've pretended nothing of the sort, neutral effects are not an explanation for the three fold expansion of the human brain from that of apes.
Genetic basis of human brain evolution overall about the genetics of human evolution, including the brain.

  • Human brain volume in cm^3, 1129-1685
  • Chimpanzee brain volumn, 230-415
  • Gorilla, 400-565
  • Orangatan 300-400
  • Gibbon 70-152
  • Old World Monkeys 33-205
  • New World Monkeys 4-123
(Genetic basis of human brain evolution. Fig. 2)

This anthropocentric notion is incomplete at best. First, the superior human brain is the result of progressive changes over a prolonged period of 60–70 million years in the lineage leading from ancestral primates to modern humans, although the rate of change has been particularly dramatic in the last few million years
Now that represents a burden of proof, based on genomic comparisons. Bruce Lahn, one of the authors of the paper you cited and linked had this to say about human brain evolution:

“For a long time, people have debated about the genetic underpinning of human brain evolution,” said Lahn. “Is it a few mutations in a few genes, a lot of mutations in a few genes, or a lot of mutations in a lot of genes? The answer appears to be a lot of mutations in a lot of genes. We've done a rough calculation that the evolution of the human brain probably involves hundreds if not thousands of mutations in perhaps hundreds or thousands of genes—and even that is a conservative estimate.” (Human Brain Evolution Was a 'Special Event'. HHMI)​
https://www.scientificamerican.com/article/garbled-dna-might-be-good-for-you/ how widespread significant mutations in somatic cells are in healthy people. 30% or more of your liver cells have an extra chromosome or are missing one, for example.

Bottom line:

For all these reasons, genome biologist Angelika Amon at MIT (and also a Howard Hughes scholar), whose research focuses on aneuploidy in cancer and aging, thinks that major genetic variation in healthy bodies has been overestimated. That’s in part because she thinks it is biologically implausible: Her studies shown that aneuploidy makes cells grow slowly and show signs of metabolic stress. “Everything we’ve studied about aneuploidy in yeast, mouse and humans shows us that having the wrong chromosome number is not a good thing,” she said. (Garbled DNA Might Be Good for You, Scientific American)​

https://www.nih.gov/news-events/nih-research-matters/gene-regulates-sleep-length DEC2 genetic mutation that allows for less sleep... again. The specific label for the mutant version of the gene being hDEC2. I will not stop mentioning this until you listen.

All very interesting but this one is a fairly normal protein coding gene. This mutation appears to be effecting normal circadian rhythm, not really effecting brain development or function.
 
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PsychoSarah

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All very interesting but this one is a fairly normal protein coding gene. This mutation appears to be effecting normal circadian rhythm, not really effecting brain development or function.
-_- circadian rhythm is controlled by the brain. Sleep is a brain function. But no, says the guy that acted as if metabolic disorders were the result of brain gene mutations. You like to broaden your choices when it suits you, but when it does it, you sure like to narrow your perspective. Sleep is controlled by the brain, I will not stand for your suggestion that it is not relevant to brain function when it is controlled by the brain directly.
 
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