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Author | Topic: Genetics and Human Brain Evolution | |||||||||||||||||||||||||||
eggasai Inactive Member |
quote: The Talk Origins shelf of skulls gives the illusion of a gradual anagenesis of the human skull. Homo habils had a cranial capacity just over 500cc while the Austropithecines are thought to have averaged above 400cc. The period from at least 5 mya until under 2 mya represents a prolonged period of stasis with about a 200cc variance not counting dimorphic variables. Homo habilis was most likely contemporary with Turkana Boy or only seperated by a couple of hundred thousands years. Turkana Boy weighs in at a cranial capacity above 900cc and Homo erectus cranial capacity remains static for at least 1 million years. Now, if you would like to take a walk through the shelf of skulls I would be delighted to debunk this optical illusion with substantive details. By the way, Homo rudolfensis was originally dated 3 million years old and only moved because Homo habilis was 200cc smaller. The dates assigned are obviously bogus but given what you listed, this one is a no brainer (LOL I'm so punny ). Everything from A to F is an ape, everything from G to you and me are humans. What Talk Origins fails to clarify is that the human brain is three times that of a chimpanzee.
quote: Then you should be able to tell me both the species, cranial capacity and speciman catalogue ID. I say it's either ape or human, what is your criteria for determining it is a transitional?
quote: On the contrary, I have the Chimpanzee Genome Consortioums conclusion that natural selection was not a factor in the evolution of humans from the last common ancestor of chimps and humans. I have the selective coefficients from the divergance between human and chimpanzee genomes. I have the comparative anatomy of contemporary chimanzee and human morphological traits to use as a based line. Finally I have the divergance of the respective genomes and the observed mutation rate for hominids, the fixation rate and the deleterious effects of mutations on protein coding and functional genes. I am far from incredulous and I'm immune to these Darwinian rethorical devices. The discussion can focus on circular arguements over semantical hair spliting but I'm not chasing it. I have an idea, why don't you guys just correct the errors in one anothers posts and I'll jump back into the discussion when your done. Edited by eggasai, : I wanted to rephrase something
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eggasai Inactive Member |
quote: Like I said, let me know when you guys are interested in discussing genetics and the human brain.
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eggasai Inactive Member |
quote: Homo rudolfensis KNM-ER 1470 was originally dated 3 million years old which would make it older then the australopithecines. It had to be moved up a million years because it didn't fit into the anagenesis of Darwinian naturalistic a priori assumptions.
quote: They are placed in the chart in such a way as to give the illusion of anagenesis. What you are calling a phylogenetic analysis is really Darwin's tree of life revisted. It is an a priori assumption that has no genuine frame of referance.
quote: You are trying to use a very precise measurement and apply it to skulls that are often crushed, fragmented and dated using highly subjective criteria. Cranial capacity represents a cerebral rubicon that marks a clear line of demarkation in the transition from ape to humans. The genetic basis for such a morphological innocation simply does not exist. "We’ve proven that there is a big distinction. Human evolution is, in fact, a privileged process because it involves a large number of mutations in a large number of genes,” Lahn said. “To accomplish so much in so little evolutionary time”a few tens of millions of years”requires a selective process that is perhaps categorically different from the typical processes of acquiring new biological traits.” Generally speaking, the higher up the evolutionary tree, the bigger and more complex the brain becomes (after scaling to body size). But this moderate trend became a huge leap during human evolution. The human brain is exceptionally larger and more complex than the brains of nonhuman primates, including man’s closest relative, the chimpanzee. One way to study molecular evolution is to examine changes of when and where proteins are expressed in the body. “But there are many challenges to studying the evolution of protein expression. Instead, we chose to track structural changes in proteins,” said graduate student Eric Vallender, lead author of the article along with former graduate student Steve Dorus, who both work with Lahn. The researchers examined the DNA of 214 genes involved in brain development and function in four species: humans, macaques (an Old World monkey), rats and mice. (Primates split from rodents about 80 million years ago; humans split from macaques 20 million to 25 million years ago; and rats split from mice 16 million to 23 million years ago.)" http://chronicle.uchicago.edu/050106/lahn.shtml
quote: No I'm not, I'm making a very specific inferance based on what science is telling us about this supposed transitional. The brain would have had to triple in size in about 1.5 million years from Homo habilis 510cc and modern humans 1350cc. This become increasingly ridiculas when you look at the actual genes involved. Do you realize that most of the neural genes would require in-frame indels of considerable length. Brain genes are amoung the most highly conserved genes in the human body, a close second would be the liver which would have underwent intense adaptive evolution as well. Random mutations plus natural selection are obviously not going to get you where there. Relaxed funtional constrait does not make any sense because of the deleterious effects. Then there is the fact that these would have to be germline mutations during the cleavage stage and it is here that mutations are least likely to occur. Now you can use all the scattergrams and tree like charts you like. The genetic basis such such a morphological giant leap does not exist except in the mind of Darwinians.
quote: What you are doing here is pouring the concrete before the frame is ready. EQ is fine for making precise measurements but we really don't have those from prehistory, for one thing the dates are highly subjective. That said, do you really think it makes sense to compare Homo habilis (actually an austropithcine if you mean OH62) to a gorilla? Why don't you do you little formula for a chimpanzee? I think you will find that Homo habils is just a little bigger.
quote: You can't compare the adaptation of a limb to the complete overhaul of neural genes, it has no rational basis: "“The making of the large human brain is not just the neurological equivalent of making a large antler. Rather, it required a level of selection that’s unprecedented,” Lahn said. “Our study offers the first genetic evidence that humans occupy a unique position in the tree of life. Simply put, evolution has been working very hard to produce us humans.” " (from the article linked above)
quote: The absolute values are of paramount importance whether they interest you or not. They are crucial because your explanation of natural selection would not have been a big factor. "Although it is more difficult to quantify the expected contributions of selection in the ancestral population, it is clear that the effects would have to be very strong to explain the large-scale variation observed across mammalian genomes. There is tentative evidence from in-depth analysis of divergence and diversity that natural selection is not the major contributor to the large-scale patterns of genetic variability in humans." (Chimpanzee Genome Consortium, Nature 2005) Charles Darwin when he wrote On the Origin of Species proposed that natural selection was the primary mechanism for adaptive evolution. In this day and age it's the first thing the evolutionists use to explain a major mophological adaptation. How did we get here? Darwin's On the Origin of Species is just one long arguement against 'special creation'. It's not a genetic mechanism, it's rethoric used as a dialectical tool meant to seperate people from belief in 'special creation', nothing more. Want to show me I'm wrong, no problem. Let's take a walk through that actual scientific research. We can look at the Chimpanzee Genome paper, some of Bruce Lahn's work and the allometry of Asian Homo erectus skulls compared to modern Chinese. I'm telling you before we start, the transtion from Homo habilis to Homo erectus didn't happen and the evidence is telling us exactly that. Edited by eggasai, : transcript error having a deleterious effect on my post
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eggasai Inactive Member |
On the contrary, I have the Chimpanzee Genome Consortioums conclusion that natural selection was not a factor in the evolution of humans from the last common ancestor of chimps and humans.
quote: "Although it is more difficult to quantify the expected contributions of selection in the ancestral population, it is clear that the effects would have to be very strong to explain the large-scale variation observed across mammalian genomes. There is tentative evidence from in-depth analysis of divergence and diversity that natural selection is not the major contributor to the large-scale patterns of genetic variability in humans." (Chimpanzee Genome Consortium, Nature 2005) Maybe you should read my posts and the scientific literature a little more carfully. Edited by eggasai, : Transcript error
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eggasai Inactive Member |
"Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins, as listed in Supplementary Tables 4 and 5)."
The International Chimpanzee Chromosome 22 Consortium, Nature 27 May 2004 These are inframe indels in protein coding genes, notice it's 20.3% of the ones on PTR22. Actually these are just differences in side by side comparision but when assuming a common ancestor it must have been an indel that produced it.
quote: What it contradicts is the a priori predictions of Darwinians who expected anagenesis progressions rather then a major overhaul of protein coding genes. That isn't near as astonishing as the inframe indels that would be required in the regulatory genes or the outliers, particularly the ones that are functionally biased in crucial neural development.
quote: It seems as obvious as it needs to if you are aquainted with the scientific literature on the subject. Why don't you google mutations and human neural genes or just read some of the papers I often quote, cite and link.
quote: The only times that relaxed functional constraint is obsered is rare instances where it improves the enzymes ability purge transcript errors. The only reason that the mutation rate is not 0 is because of the physiological costs of adaptation. Relaxed funtional constraint, 'by it's nature' runs the risk of severly deleterious effects due to an increase in the number of them. I fail to accept the logic you are using because...how can I say this nicely... it oversimplifies things way too much.
quote: "The diversity of the earliest stages of development, here illustrated strictly within the vertebrates, provides one of the strongest challenges to the neo-Darwinian conception of homology and macroevolution. Given the hierarchical, step-wise logic or "architecture" of animal development, early stages such as cleavage and gastrulation lay the groundwork for all that follows. Body plan structures in the adult, for example, trace their cellular lineage to these early stages. Thus, if macroevolution is going to occur, it must begin in early development. Yet it is precisely here, in early development, that organisms are least tolerant of mutations. Furthermore, the adult homologies shared by these vertebrates commence at remarkably different points (e.g., cleavage patterns). How then did these different starting points evolve from a common ancestor?" http://www.arn.org/docs/odesign/od182/hobi182.htm
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eggasai Inactive Member |
quote: You are obviously confusing overall divergance with comparisons of genes. The 95% is overall, the protein coding genes show differnces at an amino acid sequence level in 83% of the protein codeing genes. In the Chimapnzee Chromosome 22 paper the found gross stuctural changes would have been required in 20% of the genes.
quote: I keep going over the same ground because you don't ask questions you just contradict me. The amino acid sequence diverge which is clearly an indication that the amino acid sequences would have had to change, that's the point. Eventually I will get into applying this to the known mutation rate but it's going to take a lot longer then usual since you are unfamilar with comparitive genomics.
quote: Again, that's 29% of the protien coding genes are identical. With 35 million nucleotide substitutions, 5 million indels totalling 90 Mb and 20 Mb worth of chromosomal rearrangements in 9 pericentric inversions. That comes to 145 Mb that have to diverge in 7 million years with hundreds if not thousands of mutations in hundreds if not thousands of genes. In 7 million years it would require 20 mutations fixed in the respective genomes per year for 7 million years. Again, you have confused the amount of divergance with the percentage of protein coding genes that are identical. If you would stop trying to make me feel like I don't know what I'm talking about I'll break down the particulars to you. Untill then we will just have to keep this volleyball thing up.
quote: The probability argument is worse then useless, they never attempted anything like that. The simply said that they attributed the divergance in the genes to regional variation.
quote: I don't know what the point of that was and I'm not sure you do either.
quote: I don't know what you used to calculate the number of fertilization events but there are 350,000 generations (est. 20 years) in 7 million years of continutous evolution. We have no idea if the indels, some as long as a million bps long, were all one time events. They indentified 5 million differences totalling 90 Mb. They averaged 300 bp and they were found mostly in alu elements but also in protein codeing, regulatory and outlier genes. You really should read the Chimpanzee Genome Consortium's paper.
quote: With a mutation rate of 2 x 10^-8 it's 2 mutations per 100,000,000 with approximatly 3 billion nucleotides in the respective genomes (actually 2.74 billion). That comes to 60 mutations per diploid generation so you double it, which comes to 120 per generation. You probably have anywhere from 120-170 germline mutations in you own copy of the genome. Most of them, and I do mean virtually all, do nothing at all because they are either in the junk DNA or they don't change functionally important genes. If you had one in one of the regulatory genes involved in the development of your neocortex you would never have been born. This might take longer then usuall but we will get there, trust me.
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eggasai Inactive Member |
quote: You seem to be confusing the inframe indels with the gross structural changes that would be required in the protein coding genes discussed in the Chromosome 22 paper. I don't know why you are so indent of conflating the evidence but I suppose it's just a diversionary tactic. It would really help you if you learned to focus on one thing at a time.
quote: I was talking here about the HAR1 regulatory gene, it's 118 nucleotides long and 18 of them diverge between chimps and humans. You are going off on somekind of a tangent here and making vauge references to a paper, maybe you should quote it at least.
quote: The papers themselves are being ignored since you seem intent on talking in generalities. You blew by my point about the mutation rate reguired for 145 Mb worth of divergance. That still comes to a mean average of 20 per year for 7 million years. Then it stops in modern times and levels off at 2x10-8 which it 2 per 100,000,000 nucleotides per diploid generation. The problem is that you don't want to actually look at the evidence. I assume by your response that you either don't intend to look up the affects of mutations on functionally biased neural genes or you don't want to talk about them.
quote: You asked about the cleavage stage so I went ahead and linked you to a paper that showed a typical Darwinian picture of it. You keep missing my points because you don't like going into the specifics. You want to know what my argument here is in comprehensive terms? Here you go. 145 Mb diverge in 7 million years is far beyond the range of the observed mutation rate. It comes to 20 million nucleotides per year for 7 million years. With human populations at about 6 billion our geneomes diverge by 1/10 of 1% and are rarely fixed. The physiological costs of the human brain growing from that of an ape is enormous and refutes Darwinian anagenesis scenerios completly: "For example, in comparison with chimpanzees, the brain weight of humans is 250% greater while the body is only 20% heavier (MCHENRY 1994 ). The dramatic evolutionary expansion of the human brain started from an average brain weight of 400-450 g 2-2.5mya million years (MY) ago and ended with a weight of 1350-1450 g 0.2-0.4 MY ago" (Evolution of the Human ASPM Gene, a Major Determinant of Brain Size (Genetics 2003)) The Human Accelerated Regions are being explored and allready a regulatory gene involved in the development is known to diverge by 18 nucleotides in a gene only 118 nucleotides long. There is no explanation for this naturally occuring and random mutations would be deleterious. The only way would be for the genetic mechanism for altering the amino acid sequence to be identified. That's the primer but this thread has bounced around so much getting to the actual evidence doesn't likely. I'll give it some time but you don't seem to believe me when I tell you I am not the run of the mill creationist you are use to dealing with. No matter, let's see what you can do with this post.
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eggasai Inactive Member |
quote: The study was not limited to macaques, he made broad comparisons: "Human ASPM has 28 coding exons, spanning 62 kb in chromosome 1p31 and encoding a huge protein of 3477 amino acids (Fig 1). I determined the entire coding sequences of ASPM from one human, one chimpanzee, and one orangutan, and compared them in the phylogenetic tree of the three species" (Evolution of the Human ASPM Gene, a Major Determinant of Brain Size (Genetics 2003)) He has done a number of papers on the subject and since you are going by a news item it's no wonder you got confused.
quote: You still haven't got the big picture here, the paper is available online, why don't you google it?
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eggasai Inactive Member |
quote: Nothing could be farther from the truth. You guys have not even bothered to read the paper the news release is based on. I would have been happy to provide quotes, citations and links early in the thread but I don't think I will now. The errors in this thread are appearing in virtually every post but most of them are not mine. You only made one correction that stood up to close scrutiny.
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eggasai Inactive Member |
quote: Ok, fine...
quote: Sounds pretty reasonable.
quote: There are two issues here, one is the total amount of evolution going back 25mya and the divergance between chimpanzees and humans. You have to understand, a primate brain is roughly 3 times bigger then an ordinary mammals and the human brain is roughly 3 times bigger then an apes. The quote from the press release was just a little hyperbole to get your attention. I was hoping to get into the direct comparison of genes and Lahn has done several comparisons along those lines.
quote: First of all there are less then 20,000 genes, the 35,000 is from a rough estimate immediatly following the HGP initial sequence. Roughly 1% of the human genome is believed to code for proteins, there are another 3-4% that are funtionally important gene (outliers, regulatory genes, housekeeping genes). Most of the mutations that have a strong enough effect (3 out of 4) are going to be deleterious. You do see some of this in modern biology in the immuity system and other places. My guess is that there are transposable elements that have to be altered in order to adjust for viruses and such. That's just a guess but that is one of the things I am most curious about. Mutations are truely random and most of them are the result of transcript errors. Remember when I was talking about the central dogma of biology being DNA-transcription-RNA-translation, that's why I brought it up. The DNA is transcribed and goes through various cell cycle stages where transcript errors are corrected or the cell dies. We can get into that later, what is important here is that transcript errors and a failure to correct them is what causes most mutations like the ones in you and me. The only way that they are inheritable is if the are germline mutations and the genome is most vulnerable in the early stages of development. That's why I brought up the cleavage stage, that's the time and place where major changes would have to be made.
quote: What I said was that there were 145 Mb (million base pairs)that diverge between chimpanzees and humans. I gave 7 million years for that to happen and it comes to just over 20 bps per years as a mean average. There are 350,000 generations in that time when you estimate a generation at 20 years. The mutation rate is roughly (2x10^-8 which would be 2 for every 100,000,000 bps. This would come to about 120 bps per diploid generation and observed mutations is usually anywhere from 120 to 180bps. I won't get into the fixation rate now except to say they are rarely fixed in successive generations.
quote: When we talk about 145 Mb we are talking about then split between the two genomes. The thing is that mutations happen during meiosis so there are two copies of the chromosomes so it stands to reason that there are twice the number of transcript errors. I understand what you are saying but it gets complicated when you are talking about whether the difference between the two genomes is the result of one geneome being altered or the other. I have a much simplier way of approaching it. The chimpanzee genome paper looks at a side by side comparison of chimpanzee and human genomes. This gives us the divergance and it comes to about 16 million substitutions in the two genomes or 35 million nucletides measuring the total amount of divergance. There are about 45 million bases in each of the two genomes for a total of around 90 Mb. The chromosomal rearrangements are simply inversions, the chimpanzee goes 1,2,3... and the human seqment goes 3,2,1. The idea is that they simply flipped but the ones the Chimpanzee Genome Constortium looked at were as long as 4 Mb.
quote: Sounds good, I look forward to the next round of questions. If you like I can put together an annotated bibliography on the papers I am referancing. When you are looking at scientific literature it's not hard to make mistakes, scientists do it all the time. What is important is that what is clear should come front and center. I think it will help a lot if we took a good look at the Chimpanzee Genome paper and some of the comparisons they made.
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eggasai Inactive Member |
I've been doing this for a couple of years and probably corrected more errors in this thread then I have that entire time. I've never seen so many basic misconceptions and the papers have not been quoted, cited are linked in any of your posts. You don't seem to be doing anything other then tell me I'm wrong which is nothing more then ad hominem rethoric.
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eggasai Inactive Member |
quote: So you respond with this little quip...
quote: I know what the problem is, you don't know what a reading frame is. Those are the protein coding genes, a gross stuctural change is nothing more then 20% of the protein coding genes are much more different then predicted.
quote: That's exactly right and your problem would be...?
quote: An indel is just a mutation of length and a reading frame is just the the amino acid sequence. You seem to think that a reading frame is like the rack on a pool table that puts the balls in a triangle. It's not and until you start to realize that this is just a difference in the amino acid sequence you are going to keep correcting me based on your own misconception.
quote: You don't realize that the regulatory genes come in amino acid sequences do you? When 18 nucleotides diverge that means that at least 6 amino acids are different. The nucleotides don't code for anything, the amino acid sequences are the code for proteins.
quote: I don't really need to look back, it's just been one misconception after another. It would be nice if you guys were intent on actually correcting errors instead of unanimously contradicting me, whether I'm right or not.
quote: What that counts is 35 million single nucleotide substitutions, those are the only ones measured in nucleotides. The indels and chromosomal rearrangements are measured in base pairs. Now as far as mutations that involve in hundreds of millions of base pairs or nucleotides then I want to see it. Technically, the chromosome 2 fusion would not even be considered a mutation since the sequence didn't actually change. Just in case you really are on to something here, tell me about the indels that mark the divergence between humans. In comparing the genomes of chimpanzees and humans the indels out numbered the indels as measured in base pairs. Does that hold true for human divergence?
quote: Because it would require 20 mutations (counting the rearrangements) per year for 7 million years. The mutation rate observed has a lot of variables but it's not the hundreds of mutations that would have had to be fixed. Much, if not most, of the divergence is fixed between humans and chimpanzees. If you don't like 2x10^-8 then try another one that adequetly fits the divergence. Let me guess, you think 400 base pairs diveging between the two genomes per generation is no big deal right?
quote: Oh really? Here is a list of known effects from mutations that involve genes in the human neural system:
Chromosomal translocations fusing the BCL6 gene to different partner loci are recurrent in primary central nervous system lymphoma and may be associated with aberrant somatic hypermutation or defective class switch recombination "The transcription factor SOX2 is expressed most notably in the developing CNS and placodes, where it plays critical roles in embryogenesis. Heterozygous de novo mutations in SOX2 have previously been associated with bilateral anophthalmia/microphthalmia, developmental delay, short stature, and male genital tract abnormalities."
Mutations within Sox2/SOX2 are associated with abnormalities in the hypothalamo-pituitary-gonadal axis in mice and humans. "Neurodegenerative disorders affecting the central nervous system, such as Alzheimer's disease, Parkinson's disease, Huntington's chorea (HD) and amyotrophic lateral sclerosis are characterized by the loss of selected neuronal populations. Another striking feature shared by these diseases is the deposition of proteinaceous inclusion bodies in the brain, which may be intracytoplasmatic or intranuclear, or even extracellular. However, the density and prevalence of aggregates are not always directly related to neurodegeneration. Although some of these diseases are the result of mutations in known proteins, with HD a clear example, the expression and location of the affected protein do not explain the selective neurodegeneration."
Cellular and molecular mechanisms involved in the selective vulnerability of striatal projection neurons in Huntington's disease. The physiological costs are enormous because the deleterious affects are devastating. The genes with a functional bias involved in neural development do not respond well to mutations. Yet, it is exactly here that adaptive evolution must develop the size and complexity that became the human brain. One thing is certain, random mutations would be deleterious most of the time and a beneficial affect from one has yet to be observed in the human brain. Edited by eggasai, : transcript errors
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eggasai Inactive Member |
Hey Steve, I wasn't able to get on CF so I've been hanging out here. At any rate, you wanted to correct something.
quote: Like counting all of the base pairs in the indels and applying them to the mutation rate as measured in base pairs.
quote: So it's insane to measure a mutation by the number of base pairs involved? Like I keep trying to tell you, they should be measured in base pairs. The average indel is something like 300 bps, your trying to tell me that every generation there was at least one fixed along with 5 single nucleotide substitutions. I'm pretty much convinced that the only mistake I'm making is introducing myself as a creationist.
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eggasai Inactive Member |
Ain't got none and he's not the first geneticist I've ran into in cyberspace.
"An open reading frame or ORF is any sequence of DNA or RNA that can be translated into a protein. In a gene, ORFs are located between the start-code sequence (initiation codon) and the stop-code sequence (termination codon). ORFs are usually encountered when sifting through pieces of DNA while trying to locate a gene. Since there exist variations in the start-code sequence of organisms with altered genetic code, the ORF will be identified differently. A typical ORF finder will employ algorithms based on existing genetic codes (including the altered ones) and all possible reading frames." Open reading frame - Wikipedia That's the point, nothing about this is all that mystical. The open reading frame is simply an amino acid sequence that can be translated into a protein. What is more a regulatory gene, unless I'm greatly mistaken. comes in amino acid sequences.
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eggasai Inactive Member |
quote: Ok, so the triplet codons in regulatory genes don't code for amino acids. A single nucleotide substitution is different from a single nucleotide polymorphism and an indel a million bps long counts as one mutation. Just tell me something, does it give you pause when you see a regulatory gene with 18 nucleotides that divergen between chimpanzees and humans? I mean especially when chickens and chimps only diverge by two and their LCA lived 310 mya. Let me guess, it doesn't supprise you one bit.
quote: Just what I said, single nucleotide substitutions and indels measured in base pairs.
quote: If you were to take all of the mutations in your personal genome and that measured them in single nucleotide/base pair increments, would the single nucleotides substitutions be greater or lessor in your genome?
quote: So you have one indel 300+ bps plus 5 single nucleotide substitutions in your genome that you will, of did, pass onto your offspring in as a permenant fixture in their genomes?
quote: I think it is a very big deal since the mutation rates I am looking at measure mutations by the base pair, not by mutational events. I am also suspect that the accumulated single nucleotide substitutions outweigh indels in length as measured in base pairs. Finally, I think most, if not virtually all the transcript errors in the germline cells are repairable in successive generations. What is really important here is that even if you are totally convinced that the divergance in the two genomes are accounted for by the observed mutation rate, it does not account for the human brain.
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