Is the Human Brain a Null Hypothesis for Darwinian Evolution?

[mark kennedy]

We have been told for decades that we are nearly identical to Chimpanzees in our DNA, it's simply not true. That is vitally important when it comes to the human brain since the genes involved in the development of the brain do not respond well to changes of any kind, especially mutations. The human brain is almost three times bigger then the Chimpanzee and there are dramatic differences in the brain related genes. With that in mind consider whether or not the evolution of the human brain from that of apes has any known molecular basis. If not, do you think this creates a logical and scientific disproof of the Darwinian doctrine that men and apes share a common ancestor?

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same. More importantly, with brain related genes I have yet to see one that had a beneficial effect. These are the effects most often seen:

Charcot–Marie–Tooth (CMT) sensorimotor neuropathy
Infantile spasms, dystonia, and other X-linked phenotypes
Schizophrenia
Brain tumors
Alzheimer's disease
Parkinson's disease​

Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.

Human Genome Project Landmark Poster

FIGURE 2. Comparative neuroanatomy of humans and chimpanzees. (Genetics and the making of Homo sapiens. Nature April 2003)

Charles Darwin in the preface to ‘On the Origin of Species’ credits Jean-Baptiste Lamarck with being the first man to propose that ‘the doctrine that species, including man, are descended from other species.’ This, Darwin argues, ‘being the result of law, and not of miraculous interposition.’ One of Darwin’s contemporaries, Gregor Johann Mendel, was doing a series of experiments with pea plants that yielded the laws of inheritance that would become the cornerstone of modern genetics. Darwin’s book popularized the idea of common decent while Mendel’s only surviving paper would not be rediscovered for nearly half a century later. Mendelian laws of inheritance became inextricably linked to waves of discovery starting with chromosome theory and culminating in the molecular basis of heredity: The DNA double helix. Darwinism contributed nothing to the waves of discovery but was philosophically commingled with genetics in what has become known as the modern synthesis.

In order to examine the scientific basis for common descent I propose to examine the genetic basis for the common descent of humans from that of apes. The most dramatic and crucial adaptation being the evolution of the human brain. Charles Darwin proposed a null hypothesis for his theory of common descent :

“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” (Darwin, On the Origin of Species)​

With a cranial capacity nearly three times that of the chimpanzee the molecular basis for this giant leap in evolutionary history is still almost, completely unknown. Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes. I propose that a critical examination of common descent in the light of modern insights into molecular mechanisms of inheritance is the single strongest argument against human/ape common ancestry.

Darwin discussed what he called the 'bane of horticulture', this was infertility. Haldane in 'The Cost of Natural Selection indicated "genetic deaths," which is either deaths or it's equivalents in reduced fertility. He said that it would take 300 generations for a beneficial mutation to become fixed with 1667 accrued in 10 million years.

Like Darwin, he used artificial selection to illustrate what would have had to happen in natural settings:

"especially in slowly breeding animals such as cattle, one cannot cull even half the females, even though only one in a hundred of them combines the various qualities desired." (Haldane, The Cost of Natural Selection)​

For us to have evolved from apes it would have required an accelerated evolution of brain related genes. The evolution of the human brain would have had to start it's accelerated evolution on a molecular basis some 2 million years ago and within Homo Erectus (considered human by most creationists) would have had a brain size twice that of the Austropihicene and early Hominids:

Early Ancestors:

A. Afarensis with a cranial capacity of ~430cc lived about 3.5 mya.
A. Africanus with a cranial capacity of ~480cc lived 3.3-2.5 mya.
P. aethiopicus with a cranial capacity of 410cc lived about 2.5 mya.
P. boisei with a cranial capacity of 490-530cc lived between 2.3-1.2 mya.
OH 5 'Zinj" with a cranial capacity of 530cc lived 1.8 mya.
KNM ER 406 with a cranial capacity of 510cc lived 1.7 million years ago.​

(See Smithsonian Human Family Tree)

Homo Erectus Skulls:

Hexian 412,000 years old had a cranial capacity of 1,025cc.
ZKD III (Skull E I) 423,000 years old had a cranial capacity of 915cc.
ZKD II (Skull D I) 585,000 years old had a cranial capacity of 1,020cc
ZKD X (Skull L I) 423,000 years ago had a cranial capacity of 1,225cc
ZKD XI (Skull L II) 423,000 years ago had a cranial capacity of 1,015cc
ZKD XII (Skull L III) 423,000 years ago had a cranial capacity of 1,030cc​

Sm 3 >100,000 years ago had a cranial 917cc

KNM-WT 15000 (Turkana Boy) 1.5 million years ago had a cranial capacity of 880cc​

(Source: Endocranial Cast of Hexian Homo erectus from South China, AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 2006)

Homo habilis that would have lived. 2.5–1.5 mya with a cranial capacity of ~600 cc. The next link would have been Homo erectus with a cranial capacity of ~1000cc. KNM-WT 15000 (Turkana Boy) would have lived 1.5 mya and the skeleton structure shows no real difference between anatomically modern humans. The skull while smaller then the average cranial capacity of humans but close to twice that of his ancestors of 2 mya.

That means for our ancestors to have evolved it would have required a dramatic adaptive evolution of the size just under 2 mya sandwiched between two long periods of relative stasis. One such gene would have been the HARf regulatory gene involved in the early development of the human neocortex from 7 to 19 gestational weeks. With only two substitutions allowed since the common ancestor of the of 310 mya the divergence between humans and chimpanzees indicates 18 substitutions as early as 2 mya. (Nature, vol. 443, no. 7108, pp. 167-172 September 14, 2006)The ASPM gene while 99.3% the same for the human–chimpanzee comparison is marked by ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume.(Genetics, Vol. 165, 2063-2070, December 2003) In addition, a total of 2014 genes or ~10% of brain related genes analyzed differed in expression between humans and chimpanzees brains.(Genome Res. 14:1462-1473, 2004 ).

Evolutionists used to be able to use a 10 million year timeline, then it was 5 million years but when it comes to the most important adaptation you are looking at less then 1 million years and realistically it's only half that.

Darwin's null hypothesis for common descent is not unanswerable:

“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” (Darwin, On the Origin of Species)​

If you take the road less traveled and choose to question common descent popularized by Darwin I submit that human brain evolution is prime topic. Darwin's theory is supposed to absolutely break down if a complex organ by decent with modification. My proposal is simply this, the human brain had neither the time nor the means to have evolved from that of apes.

Grace and peace,
Mark

 

[lesliedellow]

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same.

Then how come we share 60% of our genes with fruit flies? I imagine that even creationists would sooner have a chimpanzee for their cousin, rather than a fruit fly.

 

[SkyWriting]

We have been told for decades that we are nearly identical to Chimpanzees in our DNA, it's simply not true.

Even if it was true, DNA is simply a building block of code.

 

[SkyWriting]

Then how come we share 60% of our genes with fruit flies? I imagine that even creationists would sooner have a chimpanzee for their cousin, rather than a fruit fly.

What if the building blocks are 60% the same. No big deal.

 

[mark kennedy]

Then how come we share 60% of our genes with fruit flies? I imagine that even creationists would sooner have a chimpanzee for their cousin, rather than a fruit fly.

There are only 4 Nucleotides that make up the two base pairs, so all genomic codes with be at least 25% the same. What the comparison is telling us is that of the 20,000 or so genes, the remainder of the comparative genes experienced at least one mutation per lineage. In other words, 70% of the genes in each species would have to experience mutations. If you know anything about mutations it's that most of the are deleterious (harmful), almost 98%. This requires an impossible number of changes in highly conservative genes resulting in fully functional reading frames which almost never happens.

With brain related genes, it simply never does.

Grace and peace,
Mark

 

[mark kennedy]

Even if it was true, DNA is simply a building block of code.

You have to understand what the DNA sequence builds and how. In protein coding genes they are built in blocks of three (triplet codons), these are formed into the 20 amino acids of life:

These Amino Acids are formed into reading frames that are translated into proteins, thus, protein coding genes. Francis Crick proved that the protein coding genes were composed of triplet codons which was a key proof in demonstrating the double helix model.

You put in a substitution or delete something from the chain you most often get a frameshift, not an adaptation:

Indels involving one or two base pairs (or multiples of two) can have devastating consequences to the gene because translation of the gene is "frameshifted". This figure shows how by shifting the reading frame one nucleotide to the right, the same sequence of nucleotides encodes a different sequence of amino acids...Frameshifts often create new STOP codons and thus generate nonsense mutations. Perhaps that is just as well as the protein would probably be too garbled anyway to be useful to the cell.

Mutations

With so many of them in vitally important, highly conserved genes, the lack of an explanation for the differences is an admission they have no molecular basis for the differences. It's not proven, it's assumed.

Have a nice day
Mark

 

[Hoghead1]

There are only 4 Nucleotides that make up the two base pairs, so all genomic codes with be at least 25% the same. What the comparison is telling us is that of the 20,000 or so genes, the remainder of the comparative genes experienced at least one mutation per lineage. In other words, 70% of the genes in each species would have to experience mutations. If you know anything about mutations it's that most of the are deleterious (harmful), almost 98%. This requires an impossible number of changes in highly conservative genes resulting in fully functional reading frames which almost never happens.

With brain related genes, it simply never does.

Grace and peace,
Mark

Funny that the scientists weren't aware of all this, whereas you, a lay person, on the sidelines, were, don't you think?

 

[Gene2memE]

Comparing the human and chimpanzee genomes: Searching for needles in a haystack Ajit Varki and Tasha K. Altheide

Abstract: The chimpanzee genome sequence is a long-awaited milestone, providing opportunities to explore primate evolution and genetic contributions to human physiology and disease. Humans and chimpanzees shared a common ancestor ∼5-7 million years ago (Mya). The difference between the two genomes is actually not ∼1%, but ∼4%—comprising ∼35 million single nucleotide differences and ∼90 Mb of insertions and deletions. The challenge is to identify the many evolutionarily, physiologically, and biomedically important differences scattered throughout these genomes while integrating these data with emerging knowledge about the corresponding “phenomes” and the relevant environmental influences. It is logical to tackle the genetic aspects via both genome-wide analyses and candidate gene studies. Genome-wide surveys could eliminate the majority of genomic sequence differences from consideration, while simultaneously identifying potential targets of opportunity. Meanwhile, candidate gene approaches can be based on such genomic surveys, on genes that may contribute to known differences in phenotypes or disease incidence/severity, or on mutations in the human population that impact unique aspects of the human condition. These two approaches will intersect at many levels and should be considered complementary. We also cite some known genetic differences between humans and great apes, realizing that these likely represent only the tip of the iceberg.
​

Initial sequence of the chimpanzee genome and comparison with the human genome The Chimpanzee Sequencing and Analysis Consortium

Here we present a draft genome sequence of the common chimpanzee (Pan troglodytes). Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements. We use this catalogue to explore the magnitude and regional variation of mutational forces shaping these two genomes, and the strength of positive and negative selection acting on their genes. In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles. We also use the chimpanzee genome as an outgroup to investigate human population genetics and identify signatures of selective sweeps in recent human evolution.
​

From a press release accompanying the above study:

The consortium found that the chimp and human genomes are very similar and encode very similar proteins. The DNA sequence that can be directly compared between the two genomes is almost 99 percent identical. When DNA insertions and deletions are taken into account, humans and chimps still share 96 percent of their sequence. At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans. In fact, the typical human protein has accumulated just one unique change since chimps and humans diverged from a common ancestor about 6 million years ago.​

The bonobo genome compared with the chimpanzee and human genomes Kay Prüfer, et al

Abstract: Two African apes are the closest living relatives of humans: the chimpanzee (Pan troglodytes) and the bonobo (Pan paniscus). Although they are similar in many respects, bonobos and chimpanzees differ strikingly in key social and sexual behaviours, and for some of these traits they show more similarity with humans than with each other. Here we report the sequencing and assembly of the bonobo genome to study its evolutionary relationship with the chimpanzee and human genomes. We find that more than three per cent of the human genome is more closely related to either the bonobo or the chimpanzee genome than these are to each other. These regions allow various aspects of the ancestry of the two ape species to be reconstructed. In addition, many of the regions that overlap genes may eventually help us understand the genetic basis of phenotypes that humans share with one of the two apes to the exclusion of the other.

​

 

[mark kennedy]

Funny that the scientists weren't aware of all this, whereas you, a lay person, on the sidelines, were, don't you think?

The statements are based on the Chimpanzee Genome paper and extensive source material.

 

[mark kennedy]

Funny that the scientists weren't aware of all this, whereas you, a lay person, on the sidelines, were, don't you think?

I'm paraphrasing from the Chimpanzee Genome paper and other sources. I can't exactly do comparative genomics in my garage as a hobby, it's based on the research material available online. Apparently, Gene2memE saw fit to quote, cite and link a few:

Comparing the human and chimpanzee genomes: Searching for needles in a haystack Ajit Varki and Tasha K. Altheide

The difference between the two genomes is actually not ∼1%, but ∼4%—comprising ∼35 million single nucleotide differences and ∼90 Mb of insertions and deletions.​

​

We have been told for decades that we are 98% the same as Chimpanzees in our DNA, the evidence clearly indicates we are 96% the same at best. What they don't want you to know is that the indels represent a mutation rate that would be a formula for extinction, not adaptive evolution.

​

Initial sequence of the chimpanzee genome and comparison with the human genome The Chimpanzee Sequencing and Analysis Consortium

thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements... patterns of evolution in human and chimpanzee protein-coding genes are highly correlated[/quote]​

That's from the abstract, the direct comparison of the protein coding genes indicate 70% of the genes diverge by at least one amino acid per lineage. It comes to 40,000 mutations resulting primarily from indels. With 40 million mutation events in 5 million years that means 8 mutations per year, permanently fixed. That comes to 90 million base pairs in indels and 35 million base single base substitutions. The protein coding genes, according to another comparison show at least 20% show gross structural changes[/quote]

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins. (DNA sequence and comparative analysis of chimpanzee chromosome 22, Nature 2004)

​

From a press release accompanying the above study:

When DNA insertions and deletions are taken into account, humans and chimps still share 96 percent of their sequence. At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans. In fact, the typical human protein has accumulated just one unique change since chimps and humans diverged from a common ancestor about 6 million years ago.[/quote]
​

No different then the abstract.

The bonobo genome compared with the chimpanzee and human genomes

Kay Prüfer, et al

Abstract: Two African apes are the closest living relatives of humans: the chimpanzee (Pan troglodytes) and the bonobo (Pan paniscus). Although they are similar in many respects, bonobos and chimpanzees differ strikingly in key social and sexual behaviours, and for some of these traits they show more similarity with humans than with each other. Here we report the sequencing and assembly of the bonobo genome to study its evolutionary relationship with the chimpanzee and human genomes. We find that more than three per cent of the human genome is more closely related to either the bonobo or the chimpanzee genome than these are to each other. These regions allow various aspects of the ancestry of the two ape species to be reconstructed. In addition, many of the regions that overlap genes may eventually help us understand the genetic basis of phenotypes that humans share with one of the two apes to the exclusion of the other.​

​

I haven't been able to find this one, I did find an article:

They found that the Ulindi's genome is about 99.6 percent identical to the chimpanzee genome and 98.7 percent identical to the human genome (Unraveling the Bonobo's Genome, and its Secrets)​

The Chimpanzee Genome paper is saying 96% counting indels, the only way the Bonobo and the Troglodyte are less like one another then either one is to humans is if you ignore the indels. Those two species can still interbreed, the statement has to be qualified and taken in context. I'll get to that when I find a copy of the actual paper and I'm not limited to these cute and paste abstractions.

Have a nice day
Mark

 

[Gene2memE]

Genetic basis of human brain evolution Eric J. Vallender, Nitzan Mekel-Bobrov, and Bruce T. Lahn

Abstract:
Human evolution is characterized by a rapid increase in brain size and complexity. Decades of research have made important strides in identifying anatomical and physiological substrates underlying the unique features of the human brain. By contrast, it has become possible only very recently to examine the genetic basis of human brain evolution. Through comparative genomics, tantalizing insights regarding human brain evolution have emerged. The genetic changes that potentially underlie human brain evolution span a wide range from single nucleotide substitutions to large-scale structural alterations of the genome. Similarly, the functional consequences of these genetic changes vary greatly, including protein-sequence alterations, cis-regulatory changes and even the emergence of new genes and the extinction of existing ones.

...snip...

There is a pervasive notion that the human brain is a qualitative break from all other species. By this notion, only the human brain can be placed in the ‘superior’ category whereas the brains of the other species can all be relegated to one ‘less-evolved’ group. 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 [89–91]. As such, species that branched off more recently from this lineage, such as apes, tend to possess larger and more complex brains than species that branched off at earlier stages, such as New World monkeys. Second, mammals in general, and birds to some degree, exhibit a trend of brain expansion over evolutionary time that is absent in other vertebrates[89]. Thus, humans are not the only species that have experienced brain expansion.

The view that the human brain is the result of a trend also affecting other primates is consistent with many studies. Both large-scale surveys of evolutionary changes in brain-related genes, in addition to studies of many single genes such as ASPM, microcephalin, SHH and GLUD2, have shown that these genes experienced adaptive evolution in various time periods along the lineage leading to humans, often affecting humans and other related primates rather than being specific to humans only. Thus, available data point away from the anthropocentric notion of human brain evolution to a more nuanced view, which sees the human brain as resulting from a trend of increasing size and complexity that also affected other living primates, although the impact on humans is undoubtedly most profound. More plainly stated, the salient features of the human brain did not all come about in the terminal human branch after divergence from chimpanzees. Rather, many changes have occurred in much earlier stages of the human lineage. Given this new view, genetic studies of human brain evolution should focus on comparisons across many primates and even non-primate species instead of being limited to only comparing humans and chimpanzees.
​

Genetic correlates of the evolving primate brain Eric J. Vallender

...snip...

Despite inferences elsewhere there is no reason to believe that the molecular evolution of the primate, or human, brain is inherently any different than the genetic evolution of any other character or trait. The brain, as a complex system, may be inclined towards certain categories of change, but it is governed by the same factors that are seen elsewhere.

...snip...

Building on the work of others (Ohno, 1972), in 1975 King and Wilson (King and Wilson, 1975) noted that “The organismal differences between chimpanzees and humans would then result chiefly from genetic changes in a few regulatory systems, while amino acid substitutions in general would rarely be a key factor in major adaptive shifts.” Little has occurred in the intervening years that would force us to reassess this basic belief.
​

 

[mark kennedy]

Genetic basis of human brain evolution Eric J. Vallender, Nitzan Mekel-Bobrov, and Bruce T. Lahn

Abstract:
Human evolution is characterized by a rapid increase in brain size and complexity. Decades of research have made important strides in identifying anatomical and physiological substrates underlying the unique features of the human brain. By contrast, it has become possible only very recently to examine the genetic basis of human brain evolution. Through comparative genomics, tantalizing insights regarding human brain evolution have emerged. The genetic changes that potentially underlie human brain evolution span a wide range from single nucleotide substitutions to large-scale structural alterations of the genome. Similarly, the functional consequences of these genetic changes vary greatly, including protein-sequence alterations, cis-regulatory changes and even the emergence of new genes and the extinction of existing ones.

...snip...

There is a pervasive notion that the human brain is a qualitative break from all other species. By this notion, only the human brain can be placed in the ‘superior’ category whereas the brains of the other species can all be relegated to one ‘less-evolved’ group. 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 [89–91]. As such, species that branched off more recently from this lineage, such as apes, tend to possess larger and more complex brains than species that branched off at earlier stages, such as New World monkeys. Second, mammals in general, and birds to some degree, exhibit a trend of brain expansion over evolutionary time that is absent in other vertebrates[89]. Thus, humans are not the only species that have experienced brain expansion.

The view that the human brain is the result of a trend also affecting other primates is consistent with many studies. Both large-scale surveys of evolutionary changes in brain-related genes, in addition to studies of many single genes such as ASPM, microcephalin, SHH and GLUD2, have shown that these genes experienced adaptive evolution in various time periods along the lineage leading to humans, often affecting humans and other related primates rather than being specific to humans only. Thus, available data point away from the anthropocentric notion of human brain evolution to a more nuanced view, which sees the human brain as resulting from a trend of increasing size and complexity that also affected other living primates, although the impact on humans is undoubtedly most profound. More plainly stated, the salient features of the human brain did not all come about in the terminal human branch after divergence from chimpanzees. Rather, many changes have occurred in much earlier stages of the human lineage. Given this new view, genetic studies of human brain evolution should focus on comparisons across many primates and even non-primate species instead of being limited to only comparing humans and chimpanzees.
​

Genetic correlates of the evolving primate brain Eric J. Vallender

...snip...

Despite inferences elsewhere there is no reason to believe that the molecular evolution of the primate, or human, brain is inherently any different than the genetic evolution of any other character or trait. The brain, as a complex system, may be inclined towards certain categories of change, but it is governed by the same factors that are seen elsewhere.

...snip...

Building on the work of others (Ohno, 1972), in 1975 King and Wilson (King and Wilson, 1975) noted that “The organismal differences between chimpanzees and humans would then result chiefly from genetic changes in a few regulatory systems, while amino acid substitutions in general would rarely be a key factor in major adaptive shifts.” Little has occurred in the intervening years that would force us to reassess this basic belief.
​

Are you just going to cut and paste abstracts? I've read them, several times years ago, have you? The King/Wilson paper btw is grossly outdated to say nothing of way off the actual overall divergence. It's like that Gorilla gene map paper you spammed without comment, it's a selective comparison.

Have a nice day
Mark

 

[Gene2memE]

Just letting the existing science speak for itself. It appears that molecular biologists have no issue with the evolutionary timeframe of human brain evolution.

So, in response to your question in the OP, the answer is no. Which perfectly aligns with Betteridge's Law.

 

[Papias]

Are you just going to cut and paste abstracts?
Mark

You write that, mark, when you just cut and pasted the whole OP, from the last time you posted the exact same thread, from years ago, right here: http://www.christianforums.com/thre...e-null-hypothesis-for-darwins-theory.7260803/ ???

Wow.

Remember that time, your "misunderstanding" was fully explained to you - did you forget all that?

I see you even again hid a bunch of skulls so as to misrepresent the data. Remember, that the last several times you hid data that way, it's been pointed out?

One example where you cut and pasted the same false "gap", and were corrected, is here, from 2011:

You post the "gap" Post #32:
http://www.christianforums.com/t7587649-4/#post58420143

Your misrepresentation is corrected, post #34.

Want more? A simple search using the search engine in the upper right shows plenty of times you've cut and pasted the same misrepresentations, and been corrected.

And now we have yet another of mark's cut and past misleading threads.

In Christ-

Papias

P.S. I see that you've also started another identical cut & paste thread in the Christians only section, at this link: http://www.christianforums.com/thre...l-hypothesis-for-darwinian-evolution.7947174/ mark, how many times have you cut and pasted this same misrepresentation? I've lost count, so could you help me out with a number?

 

[Loudmouth]

We have been told for decades that we are nearly identical to Chimpanzees in our DNA, it's simply not true. That is vitally important when it comes to the human brain since the genes involved in the development of the brain do not respond well to changes of any kind, especially mutations. The human brain is almost three times bigger then the Chimpanzee and there are dramatic differences in the brain related genes. With that in mind consider whether or not the evolution of the human brain from that of apes has any known molecular basis. If not, do you think this creates a logical and scientific disproof of the Darwinian doctrine that men and apes share a common ancestor?

Then what is your explanation for the human brain being bigger than the chimp brain? What is the cause?

Scientists, biologists, and neurobiologists say that the DNA sequence differences between the chimp and human genomes is responsible for the difference in brain size. What do you say?

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same.

And those that are not the same, they still share 98-99% sequence identity (on average). How is this a problem?

More importantly, with brain related genes I have yet to see one that had a beneficial effect.

Then how do you explain the human brain? Why is it different than the chimp brain, if not for the DNA mutations that separate them?

In order to examine the scientific basis for common descent I propose to examine the genetic basis for the common descent of humans from that of apes. The most dramatic and crucial adaptation being the evolution of the human brain.

The first thing you need to do is explain your position. What do you think is the reason or mechanism that causes the chimp and human brain to differ?

 

[Loudmouth]

I'm paraphrasing from the Chimpanzee Genome paper and other sources. I can't exactly do comparative genomics in my garage as a hobby, it's based on the research material available online.

The chimp genome paper is where we get the ~98% similarity for shared DNA. If you disagree with that number, then you need a different reference.

We have been told for decades that we are 98% the same as Chimpanzees in our DNA, the evidence clearly indicates we are 96% the same at best.

Both are correct. 98% similarity in the DNA that we share, and 96% overall when we add in DNA we don't share (i.e. indels). You have been told this numerous times, and here you are getting it wrong again. Why? For example:

Species A: GGACTTCGACATGGCAATAACGCGTCGTAT
Species B: GGACTTCGACAT-----TAACGCTTCGAAT

For this comparison, there are 25 bases total. There is a single 5 base indel and 2 substitutions. Of the 20 bases they share, 18 are the same for a total of 90% similarity. Overall they differ by 7 bases over 25 total for 72% similarity. Both numbers are right since they are comparing different things.

What they don't want you to know is that the indels represent a mutation rate that would be a formula for extinction, not adaptive evolution.

Is this a repeat of your usual misrepresentation of frame shift mutations? You do realize that frame shift mutations can only occur in about 3% of the genome, right? Indels that occur outside of translated mRNA can not cause a frame shift because there is no frame to shift. When DNA is not made into RNA or RNA that is not made into protein, there is no 3 base codon reading frame to interrupt. The vast majority of the human and chimp genome is not translated into proteins.

​

That's from the abstract, the direct comparison of the protein coding genes indicate 70% of the genes diverge by at least one amino acid per lineage.

Which is entirely consistent with 98% similarity.

It comes to 40,000 mutations resulting primarily from indels. With 40 million mutation events in 5 million years that means 8 mutations per year, permanently fixed. That comes to 90 million base pairs in indels and 35 million base single base substitutions. The protein coding genes, according to another comparison show at least 20% show gross structural changes

You can get gross structural changes with only a 2% difference at the sequence level.

When DNA insertions and deletions are taken into account, humans and chimps still share 96 percent of their sequence. At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans. In fact, the typical human protein has accumulated just one unique change since chimps and humans diverged from a common ancestor about 6 million years ago.

Of the proteins that are not 100% identical, they are 98-99% identical at the amino acid level. How is this a problem for the proposed 98% difference?

​

 

[Loudmouth]

What the comparison is telling us is that of the 20,000 or so genes, the remainder of the comparative genes experienced at least one mutation per lineage.

Out of how many bases/amino acids?

In other words, 70% of the genes in each species would have to experience mutations. If you know anything about mutations it's that most of the are deleterious (harmful), almost 98%.

Most mutations are neither harmful or helpful. Most are neutral.

This requires an impossible number of changes in highly conservative genes resulting in fully functional reading frames which almost never happens.

How is 2 changes every 100 amino acids or 100 DNA bases impossible?

Also, the vast majority of mutations are substitution mutations which do not change the reading frame.

With brain related genes, it simply never does.

If we find two brain related genes in two species which differ, would this disprove your claims?

 

[Loudmouth]

You put in a substitution or delete something from the chain you most often get a frameshift,

WRONG!!!!!!!!

Substitutions do not cause a frame shift mutation.

Do you still not understand this simple concept?

 

[Loudmouth]

Just so everyone is clear, thought I would show how a substitution mutation does not cause a frame shift. Since I don't want to have to deal with exon and intron editing, I picked this gene from E. coli:

ATGAATACTT TACGTATTGG CTTAGTTTCC ATCTCTGATC GCGCATCCAG
CGGCGTTTAT CAGGATAAAG GCATCCCTGC GCTGGAAGAA TGGCTGACAT
CGGCGCTAAC CACGCCGTTT GAACTGGAAA CCCGCTTAAT CCCCGATGAG
CAGGCGATCA TCGAGCAAAC GTTGTGTGAG CTGGTGGATG AAATGAGTTG
CCATCTGGTG CTCACCACGG GCGGAACTGG CCCGGCGCGT CGTGACGTAA
CGCCCGATGC GACGCTGGCA GTAGCGGACC GCGAGATGCC TGGCTTTGGT
GAACAGATGC GCCAGATCAG CCTGCATTTT GTACCAACTG CGATCCTTTC
GCGTCAGGTG GGCGTGATTC GCAAACAGGC GCTGATCCTT AACTTACCCG
GTCAGCCGAA GTCTATTAAA GAGACGCTGG AAGGTGTGAA GGACGCTGAG
GGTAACGTTG TGGTACACGG TATTTTTGCC AGCGTACCGT ACTGCATTCA
GTTGCTGGAA GGGCCATACG TTGAAACGGC ACCGGAAGTG GTTGCAGCAT
TCAGACCGAA GAGTGCAAGA CGCGACGTTA GCGAATAA


When translated into protein, this is the amino acid sequence.

MNTLRIGLVSISDRASSGVYQDKGIPALEEWLTSALTTPFELETRLIPDEQAIIEQTLCE LVDEMSCHLVLTTGGTGPARRDVTPDATLAVADREMPGFGEQMRQISLHFVPTAILSRQV GVIRKQALILNLPGQPKSIKETLEGVKDAEGNVVVHGIFASVPYCIQLLEGPYVETAPEV VAAFRPKSARRDVSE

I decided to create a substitution mutation to the T in the first line, second group (TACGTATTGG to CACGTATTGG).

The protein sequence changed by a single amino acid:

MNTSRIGLVSISDRASSGVYQDKGIPALEEWLTSALTTPFELETRLIPDEQAIIEQTLCE LVDEMSCHLVLTTGGTGPARRDVTPDATLAVADREMPGFGEQMRQISLHFVPTAILSRQV GVIRKQALILNLPGQPKSIKETLEGVKDAEGNVVVHGIFASVPYCIQLLEGPYVETAPEV VAAFRPKSARRDVSE

Used Expasy translate tool:

http://web.expasy.org/translate/

 

[mark kennedy]

WRONG!!!!!!!!

Substitutions do not cause a frame shift mutation.

Do you still not understand this simple concept?

Still playing the semantics game I see, let's work on the effect of mutations then we can tweek the terminology. Not really into the semantic hair splitting.

Just so everyone is clear, thought I would show how a substitution mutation does not cause a frame shift. Since I don't want to have to deal with exon and intron editing, I picked this gene from E. coli:

Not interested in E. coli, the subject is brain evolution and comparative genomics. Mutation rates might be of interest but it never gets that far, just gets dragged off on tangents like this one.

Out of how many bases/amino acids?

It's really irrelevant to the mutation rate.

Most mutations are neither harmful or helpful. Most are neutral.

Because most of them happen in parts of the genome where they don't effect genes.

How is 2 changes every 100 amino acids or 100 DNA bases impossible?

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?

Also, the vast majority of mutations are substitution mutations which do not change the reading frame.

They have to be or they are deleterious, the triple codon has to be preserved or you are looking at a frameshift. Your also assuming that the substitution is going to give you a functional amino acid that will also fold into a functional 3D protein. You have also failed to apply this to brain related genes, but we will get to that in time.

If we find two brain related genes in two species which differ, would this disprove your claims?

If you mean find a gene that is different in the Chimpanzee genome from a human gene, of course not. You seem to forget I am arguing for separate linage. If, on the other hand, you can find variant alleles in brain related genes in comparing human genomes to one another I'd be delighted to consider it.

As far as disproving my claims, you would first have to address them. We will wait and see if that happens.

Have a nice day
Mark