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Is the Human Brain a Null Hypothesis for Darwinian Evolution?

Can the Evolution of the Human Brain be a Basis for a Null Hypothesis of Darwinism?


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Loudmouth

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We are talking about just one, we are talking about all known cases of mutations in brain related genes. Not just deleterious but deadly.

That is false. You are forgetting about all of the mutations that separate humans and chimps with respect to those brain related genes.

Because those are not mutations, those are differences in the comparison of the sequence.

That's what mutations are, differences in sequence. Why would it matter whether natural processes produced that difference or a deity made those changes? Let's take one of the deleterious mutations that you have cited before. Are you saying that if humans purposefully produced that same change in sequence that it wouldn't be deleterious, that it wouldn't cause disease?

Because a difference in the two genomes and a genetic mutation are two very different things.

HOW??????

The end result is the exact same. Do you think there is some magic added to a substitution when a deity causes it as compared to natural processes?

You can find examples of mutations which result in beneficial effects from gene duplication, exon shuffling, variant alleles even gene expression or dominant and recessive change, that can be vehicles for an evolving genome. Not brain related cells, they are far too highly conserved.

Those beneficial mutations are the known sequence differences between the human and chimp brain related genes.

Start by trying to get the basic concept of comparative genomics down before you go on for pages correcting me and calling me a liar over something you never bothered to understand.

You can start by showing us how a deity making a sequence change will have a different result than natural processes making that exact same sequence change.

I never said there were none in the ground I said there were none in the fossil record,

THAT'S THE SAME THING!!!!!!

The fossil record is the fossils in the ground. If you want to claim that there are no chimp ancestor fossils, THEN PROVE IT. Otherwise, it is just a bare assertion.

Lucy AL 288-1, found in Hadar, Ethiopia had a cranial capacity of 410cc and dated 3.2mya is small even for a modern chimpanzee. Australopithecus afarensis: AL 288-1. The Taung Child, Taung 1, regarded simply as a chimpanzee for years had a cranial capacity of between 382-404 cc. Again, small even for a modern chimpanzee that ranges from 320cc to 480cc or right around 400cc on average. Modern human average right around 1400cc depending on who's statistical average you are looking at, Neanderthals had a cranial capacity 10% greater then our own.

From early primates to hominids and finally to Homo sapiens, the human brain has continued to grow. The volume of the human brain has increased as humans have evolved (see Homininae), starting from about 600 cm3 in Homo habilis up to 1600 cm3 in Homo neanderthalensis, which was the hominid with the biggest brain size. Brain Size Wikipedia
It is still nearly impossible to consider that Taung might just be a chimpanzee ancestor even though it's become increasingly obvious that human like features are sparse:

Citing deficiencies in how the Taung fossil material has been recently assessed, the researchers suggest physical evidence does not incontrovertibly link features of the Taung skull, or its endocast, to early prefrontal lobe expansion, a brain region implicated in many human behaviors. (Taung Skull not Humn-like 26 August 2014)
It's just not like the human brain:

As Taung provides the only purported pre-Homo fossil evidence for the suggested adaptive mechanism, we test the hypothesis that it displays these features. (PNAS 2014)
This has been going on for quite sometime:

Over the next decade, Dr. Holloway elaborated on these themes. But in 1980, Dr. Falk, then at the University of Puerto Rico, returned from her own trip to Johannesburg and announced a radically different conclusion: the Taung child’s brain and those of a half-dozen other South African australopithecines were like those of apes, not later humans. In Study of Brain Evolution, Zeal and Bitter Debate

We already showed you the data:

fossil_hominin_cranial_capacity_lg_v1-1.png

http://www.pandasthumb.org/archives/2006/09/fun_with_homini_1.html

We see overlaps from species to species and a nice steady increase in cranial capacity. All you try to do is cherry pick the data.

I am guessing that you will completely ignore this data, and then accuse us of refusing to discuss the topic. Am I right?
 
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mark kennedy

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That is false. You are forgetting about all of the mutations that separate humans and chimps with respect to those brain related genes.

I'll tell you what I think, I think these flimsy corrections are disingenuous. The differences between are not mutations, they are assumed to be the result of mutations, there is a big difference. That's why discussing virtually anything with evolutionists is always so tedious, they make fundamental errors in things like semantics and in this case, basic comparative genomics, and pretend to have proof when it's nothing more then presupposition and fallacious rhetoric.

Since I know you would never bother to find a valid definition, I'll post one. Perhaps it will elevate your thinking, but I won't hold my breath waiting on that one:

Comparative genomics is a field of biological research in which the genomic features of different organisms are compared.[2][3] The genomic features may include the DNA sequence, genes, gene order, regulatory sequences, and other genomic structural landmarks.[3] In this branch of genomics, whole or large parts of genomes resulting from genome projects are compared to study basic biological similarities and differences as well as evolutionary relationships between organisms.[2][4][5] The major principle of comparative genomics is that common features of two organisms will often be encoded within the DNA that is evolutionarily conserved between them.[6] Therefore, comparative genomic approaches start with making some form of alignment of genome sequences and looking for orthologous sequences (sequences that share a common ancestry) in the aligned genomes and checking to what extent those sequences are conserved. Based on these, genome and molecular evolution are inferred and this may in turn be put in the context of, for example, phenotypic evolution or population genetics.

2) Touchman, J. (2010). "Comparative Genomics". Nature Education Knowledge
3) Xia, X. (2013). Comparative Genomics. Heidelberg: Springer.
4) Russel, P.J.; Hertz, P.E.; McMillan, B. (2011). Biology: The Dynamic Science (2nd ed.).
5) Primrose, S.B.; Twyman, R.M. (2003). Principles of Genome Analysis and Genomics (3rd ed.).
6) Hardison, R.C. (2003). "Comparative genomics" PLOS

That's what mutations are, differences in sequence. Why would it matter whether natural processes produced that difference or a deity made those changes? Let's take one of the deleterious mutations that you have cited before. Are you saying that if humans purposefully produced that same change in sequence that it wouldn't be deleterious, that it wouldn't cause disease?

No, they are changes in the sequence due to transcription errors:

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. (Mutations)​

HOW??????

Miraculous interpolation at the original creation of life. Have you forgotten I am a creationist or do I need to define that term for you as well. They were separately created, with independent lineages and the changes represent differences that cannot be explained by a failure of DNA repair.

The end result is the exact same. Do you think there is some magic added to a substitution when a deity causes it as compared to natural processes?

There you go begging the question of proof and equivocating differences with a presupposition of exclusively naturalistic causes, i.e. mutations.

Those beneficial mutations are the known sequence differences between the human and chimp brain related genes.

Yet they never happen in nature, they are simply assumed with regards to natural history.

You can start by showing us how a deity making a sequence change will have a different result than natural processes making that exact same sequence change.

Not some deity, God. Now you can continue to chase this in circles as long as you like but resorting to an equivocation fallacy isn't science, it's supposition.

THAT'S THE SAME THING!!!!!!

Not if they are dated after the split and classified as human ancestors, it's an impossibility for them to be the same thing. It's called the law of excluded middle, a rule of logic you should have learned before trying to pass yourself off as an evolutionary apologist.

The fossil record is the fossils in the ground. If you want to claim that there are no chimp ancestor fossils, THEN PROVE IT. Otherwise, it is just a bare assertion.

Whenever a chimpanzee fossil is dug up it's automatically and invariably a human ancestor, no matter how ape-like. I did offer substantive and well established facts in evidence making my point that you abandoned in favor of the melodramatic indignation based on nothing at all.

We already showed you the data:

Again with the we and that convoluted scattergram. Unlike you I have actually studied the fossils represented in the scattergram. Since you obvious don't argue from actual fossil evidence it's predictable that the substance of your argument comes down to a jpeg. Begging the question of proof, there is a fallacy in every line now. Pull up dude, your scraping the trees as it is.

We see overlaps from species to species and a nice steady increase in cranial capacity. All you try to do is cherry pick the data.

On the contrary, I started the OP with the strongest fossil evidence I have seen, OH 4. The Toumai I found even more persuasive, just not convincing. Where does that fit into your pusillanimous scattergram?

I am guessing that you will completely ignore this data, and then accuse us of refusing to discuss the topic. Am I right?

No I'm going to continue to insist on actual definitions and offer expositions of legitimate scientific literature no matter how many fallacious, inflammatory remarks you flood the thread with.

Us huh? You got maybe two people participating in the thread besides you. Other then that you are performing in an empty theater and somewhere lurking in the shadows the Darwinians are laughing at you. They used you for years and left you here with is no real world knowledge of evolutionary biology to make pedantic arguments alone. Sad, so much time spent on this and basic terminology, as well as sound logic, still eludes you.

Have a nice day :)
Mark
 
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Loudmouth

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I'll tell you what I think, I think these flimsy corrections are disingenuous. The differences between are not mutations, they are assumed to be the result of mutations, there is a big difference.

They are not assumed to be mutations. The pattern of LTR divergence, that pattern being a nested hierarchy, demonstrates that the differences between the genomes is due to random mutations and selection. A common designer would not produce a nested hierarchy. Only evolutionary mechanisms do that.
No, they are changes in the sequence due to transcription errors:

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. (Mutations)​

No, the are due to copying errors during replication. Transcription is the process of making RNA from DNA. Transcription errors are not heritable. Mutations are heritable and they occur in DNA, not RNA.

Are you really arguing that mutations don't happen? Really? We have directly sequenced the genome of a child and that child's parents, and you know what we found? Mutations.

"Here we present, to our knowledge, the first direct comparative analysis of male and female germline mutation rates from the complete genome sequences of two parent-offspring trios. Through extensive validation, we identified 49 and 35 germline de novo mutations (DNMs) in two trio offspring, as well as 1,586 non-germline DNMs arising either somatically or in the cell lines from which the DNA was derived."
http://www.nature.com/ng/journal/v43/n7/full/ng.862.html

Miraculous interpolation at the original creation of life. Have you forgotten I am a creationist or do I need to define that term for you as well. They were separately created, with independent lineages and the changes represent differences that cannot be explained by a failure of DNA repair.

You don't seem to be seeing the problem. How would the result of a deity changing a base be any different than a random mutation?

Yet they never happen in nature, they are simply assumed with regards to natural history.

Already disproved this argument. We have the evidence that the differences between the genomes of species is due to mutations and natural selection.

Not if they are dated after the split and classified as human ancestors, it's an impossibility for them to be the same thing. It's called the law of excluded middle, a rule of logic you should have learned before trying to pass yourself off as an evolutionary apologist.

They are the same thing, Mark.

Whenever a chimpanzee fossil is dug up it's automatically and invariably a human ancestor, no matter how ape-like.

Prove it.

Again with the we and that convoluted scattergram.

Look who is avoiding the fossil evidence. That would be you, as usual.

On the contrary, I started the OP with the strongest fossil evidence I have seen, OH 4. The Toumai I found even more persuasive, just not convincing. Where does that fit into your pusillanimous scattergram?

You are avoiding the fossil evidence, as shown above.

No I'm going to continue to insist on actual definitions and offer expositions of legitimate scientific literature no matter how many fallacious, inflammatory remarks you flood the thread with.

I already gave you those definitions.
 
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USincognito

a post by Alan Smithee
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Hardly nonexistent; several examples of differences in genes between chimps and apes that illustrate a gradual, positive change. For example, SRGAP2. Other primates have a single gene; we have the original and three variations, a very clear case of duplication and point substitution mutations. Our four SRGAP2 genes result in more rapid neuron growth and a denser cerebral cortex than in any of our ape cousins.

Did you know about SRGAP2? If not, why didn't you look for evidence like this before making your claim? If so, why didn't you mention it?

I'm not sure if it was this thread or another of his recent ones with the same tired arguments, but I pointed out SRGAP2C and ARHGAP11B along with MYH16. I don't think he responded. He tends to just repeat the same stuff over and over. Most everything posted here is verbatim (including his misuse of null hypothesis) from 10 years ago.
 
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Paul of Eugene OR

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. . . . I didn't say impossible, I said the vast majority are going to be deleterious assuming they actually have an effect and even beneficial ones have a low instance of fixation. Did you read the OP or just post random questions as they occurred to you . . . .

Do you know the long term fate of deleterious mutations? Alas, they get bred out of the population by natural selection. Hence, their arrival doesn't really matter very much (except for the unfortunate individuals that get stuck with them, of course.)
 
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mark kennedy

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They are not assumed to be mutations. The pattern of LTR divergence, that pattern being a nested hierarchy, demonstrates that the differences between the genomes is due to random mutations and selection. A common designer would not produce a nested hierarchy. Only evolutionary mechanisms do that.

No comprehension or acknowledgement of what a genomic comparison actually is and some convoluted semantics, you are consistant.

No, the are due to copying errors during replication. Transcription is the process of making RNA from DNA. Transcription errors are not heritable. Mutations are heritable and they occur in DNA, not RNA.

Transcription and translation, those are the two concepts you need to wrap your mind around and then mutations being the result of copy errors. That would be progress.

Are you really arguing that mutations don't happen? Really? We have directly sequenced the genome of a child and that child's parents, and you know what we found? Mutations.

Try to wrap your mind around a very simple concept, mutations are copy errors.

"Here we present, to our knowledge, the first direct comparative analysis of male and female germline mutation rates from the complete genome sequences of two parent-offspring trios. Through extensive validation, we identified 49 and 35 germline de novo mutations (DNMs) in two trio offspring, as well as 1,586 non-germline DNMs arising either somatically or in the cell lines from which the DNA was derived."
http://www.nature.com/ng/journal/v43/n7/full/ng.862.html

Quote mining, that a new fallacy for you. Glad to see you expanding your horizons.



You don't seem to be seeing the problem. How would the result of a deity changing a base be any different than a random mutation?

He didn't, God created two separate lineages. It's called originally created kinds.

Already disproved this argument. We have the evidence that the differences between the genomes of species is due to mutations and natural selection.

Which is an effect without a cause, predictable.

They are the same thing, Mark.

The rest is close encounters of the pedantic one liners, enjoy the melt down, I know I will. You are falling farther and faster then I am used to, this is surprisingly easy.

Have a nice day :)
Mark
 
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mark kennedy

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Do you know the long term fate of deleterious mutations? Alas, they get bred out of the population by natural selection. Hence, their arrival doesn't really matter very much (except for the unfortunate individuals that get stuck with them, of course.)

With that not attached to anything relevant I'm going to wait and see if you say anything substantive. Deleterious effects are not a formula for adaptive evolution. Why don't you actually learn something about evolutionary biology and get back to me.

Have a nice day :)
Mark
 
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mark kennedy

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Hang on Adam. I think you meant the srgap2 gene. What I'm getting is 19 duplication in the human genome and none in primates. Outstanding!!!

I'm at work right now but can't wait to dig into this. Thanks

Grace and peace,
Mark
 
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AdamSK

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Right, there is a clear and short sequence of mutations to get from the original SRGAP2 to the several slight variations that humans have, and these collectively contribute to faster and denser neuron development. One of several actual examples we can show of mutations that lead to superior brain in humans.
 
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Paul of Eugene OR

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With that not attached to anything relevant I'm going to wait and see if you say anything substantive. Deleterious effects are not a formula for adaptive evolution. Why don't you actually learn something about evolutionary biology and get back to me.

Have a nice day :)
Mark

Ho hum. Deleterious effects are not the only effects, you know. There is the occasional beneficial mutation. The thing about beneficial mutations is, instead of being eliminated by natural selection, they accumulate due to natural selection. They build on each other, causing evolution to occur.
 
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mark kennedy

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Right, there is a clear and short sequence of mutations to get from the original SRGAP2 to the several slight variations that humans have, and these collectively contribute to faster and denser neuron development. One of several actual examples we can show of mutations that lead to superior brain in humans.

Dude these are comparisons, this doesn't demonstrate that the differences are caused by mutations, it assumes they must have. Actual mutations that have an effect are always deleterious:

identified large SRGAP2C and SRGAP2A events discovered via array CGH and resolved the internal deletions as specifically affecting SRGAP2C, removing exon 2 and inducing a frameshift. Rapid and accurate large-scale genotyping of duplicated genes and discovery of novel sites of interlocus gene conversion
These kind of disorders can be devastating:

We report on a female patient with early infantile epileptic encephalopathy and severe psychomotor disability possessing a de novo balanced translocation t(1;9)(q32;q13). The patient showed clonic convulsions of extremities 2 days after birth. Early infantile epileptic encephalopathy associated with the disrupted gene encoding Slit-Robo Rho GTPase activating protein 2 (SRGAP2).
Still doing the background reading but when they say fast evolving it really just means extremely different:

About 3.4 million years ago, a core duplicon on what is now called chromosome 1 in human descendants made one of its characteristic jumps, taking with it a copy of a gene known as SRGAP2. A million or so years later, it jumped again, creating a granddaughter of the original. No other mammals whose genomes have been examined to date have multiple copies of the gene, and the jumps coincide with a pivotal point in human evolution: As Australopithecus evolved into Homo habilis 2 to 3 million years ago, hominid brains were on their way to doubling in size. A Missing Genetic Link in Human Evolution

EichlerSRGAP_crop.jpg

Humans have multiple copies of a gene known as SRGAP2, which is thought to be involved in brain development. Chimps and orangutans have only one copy.​

You guys act like you don't realize, this is all just a comparison, assumed to be the result of mutations. The actual mutations produce disease and disorder if they do anything at all. This is another HAR1f gene for me, it's always nice to find another. That's why I keep coming back, someone will mention something like this thinking it's proof of positive effects from mutations, not realizing it's just a comparison.

Have a nice day :)
Mark
 
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AdamSK

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Please examine the differences between the 1 copy of the gene that chimps have and the multiple copies that we have. Even if you refuse to accept that these differences were due to mutation in humans, it is still evidence that mutations in the original gene possessed by chimps can result in a beneficial brain effect.
 
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mark kennedy

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Please examine the differences between the 1 copy of the gene that chimps have and the multiple copies that we have. Even if you refuse to accept that these differences were due to mutation in humans, it is still evidence that mutations in the original gene possessed by chimps can result in a beneficial brain effect.

No, two articles in 2012 reported, 'four human genes named SRGAP2A, SRGAP2B, SRGAP2C, and SRGAP2D, which are located in three completely separate regions on chromosome number 1.' I'm still doing the back ground reading but the core gene sequence is identical, then the additional human versions have an additional amino acids. It's assumed they are the result of mutations, they didn't prove anything by simply saying it was.

Have a nice day :)
Mark
 
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AdamSK

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Please read my post again.

It doesn't matter whether the human changes actually are mutations are not. Chimps have an SRGAP2 gene; humans have four copies with minor differences that can be produced by mutations. This is evidence that mutations can improve brain function, whether or not this is actually how the differences were produced, and negates your claim.

As an analogy, if the claim is that it impossible to walk from Detroit to Chicago, it is sufficient to show a route between the two to negate the claim. Even if you insist that everyone who claims to have ever walked from Detroit to Chicago along that path is lying, that doesn't negate that the path itself is there.
 
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mark kennedy

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Please read my post again.

It doesn't matter whether the human changes actually are mutations are not. Chimps have an SRGAP2 gene; humans have four copies with minor differences that can be produced by mutations. This is evidence that mutations can improve brain function, whether or not this is actually how the differences were produced, and negates your claim.

As an analogy, if the claim is that it impossible to walk from Detroit to Chicago, it is sufficient to show a route between the two to negate the claim. Even if you insist that everyone who claims to have ever walked from Detroit to Chicago along that path is lying, that doesn't negate that the path itself is there.
First of all I don't call people liars because I don't share their worldview or presuppositions. Darwinians do that. Secondly there seems to be a misunderstanding about c compaparative genomics. When they compare two sequences it's like layi g out two strands of beads with four different color beads. Every genome should show at least 25 percent sequence identity since there are only four base pairs. When it's a single base pair difference they call it a substitution if there is something in one but not in the other its called an indel. When you have three unique genes they call a duplication. Now I don't know what you think these novel genes do to my argument but so far I haven't actually made one yet but I will soon and often. When I first encountered the arctic code antifreeze gene and har1f it was guys like you who thought they had something and found out the inverse logic is intuitively obvious. If things alike are proof for common ancestry then differences argue against it. From the paper I'm reading:

"The ancestral protein protein sequence SRGAP2 is highly constrained based on the analysis ten mammalian lineages. With only one amino acid between human and mouse and no changes among nonhuman primates within the first nine exons of SRGAP2. This is in stark contrast to the duplicate copies. Which diverged from ancestral SRGAP2 less then 4mya but have accumulated as many as seven amino acid replacements, five for SRGAP and two for SRGAPb. Compared to one substitution. (Cell 2012)​

That is highly accelerated evolution of a highly conserved gene. The deleterious effects would have been devastating, unless you get to assume everything and have to prove nothing.
 
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