Genetics and Human Brain Evolution

I am new to the boards and I am interested in discussing the genetic basis of human evolution. I am specificlly interested in the evolution of the human brain over the last 2 1/2 million years. There are three main points of discussion I am proposing:1.The genetic changes involved in the acquisition of unique human features, such as highly developed cognitive functions, bipedalism or the use of complex language.Nature - Not FoundThey have compared the differences betwee the human genome and that of chimpanzees, these differences, attributed to mutations, can be reduced to ratios. Bear this in mind when looking at real world genetic research into comparisons of humans (homo sapiens) and our, supposedly, closest relative the chimpanzee.2. The genes involved and the number of changes that would be required for humans to evolve from apes.Evidence that human brain evolution was a spe | EurekAlert!One of the study's major surprises is the relatively large number of genes that have contributed to human brain evolution. "For a long time, people have debated about the genetic underpinning of human brain evolution," said Lahn. "Is it a few mutations in a few genes, a lot of mutations in a few genes, or a lot of mutations in a lot of genes? The answer appears to be a lot of mutations in a lot of genes. We've done a rough calculation that the evolution of the human brain probably involves hundreds if not thousands of mutations in perhaps hundreds or thousands of genes -- and even that is a conservative estimate."3. The genetic basis for the three-fold brain expansion over ~ 2 million years.Evolution of the Human ASPM Gene, a Major Determinant of Brain Size | Genetics | Oxford AcademicNo amount of random combinations of chimpanzee genes could ever produce such a change in size and complexity. The only way it could happen is thousands of mutations in thousands of genes.I proposed this in another forum and someone suggested I try here. I await your response to my proposal of a new topic of discussion.This message has been edited by eggasai, 08-18-2005 09:46 PM

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One of the main points is that humans are very very old.

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I know who Francis Collins is, he is the head of the Human Genome Project. I heard him discussing his new book on NPR, he left out some pretty important facts. First of all, the Chimpanzee Genome Project published the intitial seqeunce back in September of 2005. The found that the genomes of Chimpanzees and Humans was not 98%-99%, it was closer to 95%. What difference does that make? When you add up the single nucleotide substitutions, indels and chromsomal rearrangements it comes to 145 million base pairs. For these differences to have to accumulate would require 20 nucleotide fixed in the respective genomes, on average,for 7 million years. When Nature announced the publication of the Chimpanzee Genome they again said that 98% of the DNA was the same. There is just one problem with this, the paper says that single base substitutions (35Mb) are 1.29% and that they are dwarfed by the indels (90Mb)which are 3%-4%. With the mutation rate being about 2 * 10^-8 that means about 123 germline mutations per zygote.Don't believe me? Type 'chimpanzee genome' into your google search engine and the page announceing the paper will be at the top of the list. Then look up the Initial Sequence of the Chimpanzee Genome' (free online) and look up the indels. I would have loved it if Francis Collins had explained how this is possible but I doubt seriously he will.The human brain is 3 times the size of Chimpanzees, I don't think I will get any arguements to the contrary. Recently they started studying the Human Accelerated Regions, there are 49. The first one uncovered a regulatory gene involved in the developement of the cerbral cortex. When the human gene, 118 nucleotides long, was compared to the chimpanzee counterpart there were 18 substitutions. When the chimpanzee gene was compared to that of a chicken there were 2 substitutions. Chimps and chickens a believed to have a common ancestor 310 million years ago. The question arises how does such a highly conserved gene suddenly aquire 18 substitutions?Francis Collins is one of the world's leading genetic researchers, I would love to hear him explain this.

I didn't say kilobases I said megabases and one of hte chromsomal rearrangements is 4 Mb long. The observed mutation rate hovers around 2.5 x 10^-8 which comes to 173 germline mutations per diploid generation. 145 Mb in 7 million years comes to 20 per year, fixed withing the respective genomes for 7 million years. That's not just an arguement, it's double the mutation rate estimated for several decades now. When the divergance was thought to be 99% the mutation rate dovetailed nicely but now it is impossible.All the arguement I really need is take the mutation rate, estimated time frame and the amount of divergance.

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The one discursive point you have raised is how Har1 has evolved so rapidly in humans. The obvious answer would be that the gene was subject to some selective pressure which favoured its divergence from the conserved sequence, either that or it was released from some strongly stabilising negative selective pressure.

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You left out the part where you tell me how the mutation got in there without killing off the offspring.

The fact is that the standard line has been that the DNA is 99% the same in chimpanzees and humans. When it was discovered over the last 5 or 6 years, that it's actually 95%, no one seemed supprised. Because of the indels the amount of known divergance went up by between 3-4%. I am actually talking to a geneticist who says that it's no big deal, I don't see how 100 million base pairs is no big deal.There are a lot of variable in the mutation rate, that's not really the issue here. The observed mutation rate, measured in base pairs is not going to get you 300 germline mutations permenantly fixed for 7 million years. I'm trying to tell you that this simply does not happen.

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The problem with such a simple formulation is that it is in fact overly simplistic.

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It does not matter how you work the formula, the number of mutations required does not even come close to what actually happens. I cannot find an estimate of a mutation rate in any living system that nets that many germline mutations per diploid generation.

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I'm not sure why this is necessary in the absence of any evidence suggesting that such a mutation would be lethal. At best you have the indirect evidence that the 118bp non-coding region has been highly conserved in a number of vertebrate species, this is not the same as showing that any of the substitutions in the human gene are lethal in other animals. Indeed if you look at the supplementary data you will see that at least 3 of the mutations in the human are found in other species, and on assumes without lethal consequences and there are a further ten mutations seen in other species which are not present in the human gene. So at present there is no evidence to suggest that theHar1 region cannot accept a number of mutational changes without any lethal effect on offspring.

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We don't know, nor should we assume, that the 18 nucleotides in question are the result of mutations. Every time a nucleotide is substituted there is the danger of disease, defect or death. The nucleotide throws off the amino acid seqeunce, which throws off the protein seqeunce. That usually results in the reading frame being shut down, this one has 18 nucleotides that diverge between chimpanzees and humans. Mind you, this is in a crucial time of development, the cerbral cortex does not respond well to mutations in the regulatory genes. I see no reason that one cannot logically conclude that the differences are better accounted for by design rather then spontaneous mutations.You say there are three mutations in other species. Are you describing a functional gene that remains the same in successive generations or an altered gene in a minority of the population?

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Lining up 3 billion bits of genetic code, the chimp genome team determined that 96 percent of the protein-coding genes in both chimps and humans were identical, while in some stretches of DNA where genes either regulate other genes or whose function is unknown, as much as 99 percent of the genetic material in both is identical, the scientists concluded.

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I want to take another look at the original post but this one caught my attention. You are quoting from a news article based on a limited study. Why don't you check out the Initial Sequence fo the Chimpanzee Genome (Nature, 2005). They found that 29% of the protein coding genes were identical, not 96%. If you want to track it down it will give you something more current and definitive then the news article you are gleaning from.I'll check back later and if you haven't responded I'll just edit and expand this post.

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Eggasai, you are completely wrong here. The Nature article cites a total nucleotide divergence of around 4%; 1% caused by 35 million substitution mutations, and 3% caused by a total of 5 million indel mutations.

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You are confusing the actual paper with the Nature webpage announcing the paper. Type 'chimpanzee genome' into google and this will be at the top:"What makes us human? We share more than 98% of our DNA and almost all of our genes with our closest living relative, the chimpanzee. Comparing the genetic code of humans and chimps will allow the study of not only our similarities, but also the minute differences that set us apart."Chimp genome : Web focus : Naturemick is completely wrong about what I said. I said that Nature claimed 98% of the DNA in chimpanzees and humans is the same in the announcement of the Chimpanzee Genome paper that said 95%.Before you go around telling people I'm wrong you should be clear what it is I actually said. Did you even read the paper? If so do you think that a KA/KS > 1 in 600 genes and 40,000 amino acid seqeunces substituted is in keeping with the observed mutation rate in hominds?Also, the 5 million mutations you are glossing over total 90 Mb and dwarf the single substitutions. You are contradicting me and you have only read the abstract? You have to be putting me on, I've been going over this paper with one of the authors for months. Edited by eggasai, : Missed a point

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Eggasai, you are completely wrong here. The Nature article cites a total nucleotide divergence of around 4%; 1% caused by 35 million substitution mutations, and 3% caused by a total of 5 million indel mutations.

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What I said was that the Nature webpage announcing the Chimpanzee Genome paper claimed 98% of the DNA was the same, when the paper said 95% counting indels.

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You appear to have cherry-picked the lowest measure of identity you could find in the article (29%) in order to bolster your case. However that is the percentage of whole proteins (not nucleotide positions) which are identical in terms of their complete amino acid sequence.

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Oh for goodness sakes, I don't know what got you so turned around but here are a couple of choice quotes:"Orthologous proteins in human and chimpanzee are extremely similar, with 29% being identical and the typical orthologue differing by only two amino acids, one per lineage."They are different at an amino acid seqeunce level which means that the proteins are coded differently. A single nucleotide seqeunce can shut a reading frame down, which is why a codon out of place is not just a minor variation it's most likely going to be deleterious. You do know that groups of three nucleotides are triplet codons designating the amino acid right? Then the amino acid seqeunces are translated into proteins, they are talking about amino acid sequences. They are saying that taken together 29% of the protein coding genes differ by two amino acids.I have no idea where you got the whole protein thing but it's wrong.

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Just to repeat what the Nature article actually says: Around 96% of the total genome is identical (not 29% as you imply). These differences were caused by a total of 40 million mutation events (not 145 million, as you claim)

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Wrong again! They said that there 35 Mb of single nucleotide substitutions and 5 million indels and 'verious chromosomal rearrangements'. In the paper they discuss the indels that are 90 Mb taken together and more or less evenly split between the chimpanzee and human genome. There is an additional 9 chromosomal rearrangements 2 Mb to 4 Mb long totally around 20 Mb. Taken together this comes to 145 Mb.

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Anyway, if the fact that 29% of whole proteins are identical in human and chimp seems low to you, you should spend a moment considering the implications. According to the Nature article, the remaining 71% of proteins differed by an average of only two amino acids. The average length of a protein is around 1000 amino acids. This means that the probability that an amino acid from a chimp protein is identical to the corresponding amino acid in the human orthologue is equal to : (0.29 * 1.0) + (0.71 * 998/1000) = 99.858%.

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What about the probablity of a single amino acid substitution being anything other then delerious? When you add up all the amino acid seqeunces that diverge we are talking about 40,000 aminio acid sequences. That comes to at least 120,000 nucleotides and like I told you earlier a single nucleotide substitution can shut down the reading frame. The chances of an amino acid seqeunce turning into one of the amino acids of life is less then one in three. There are 20 amino acids in all living things, there are 4 nucleotides that are used to make them. 4^4 is 64 and there are 20 amino acids so that's about a 1/3 ratio. I'll give you the rest of your biology primer when you digest that much.

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If (as seems likely) the probability that human and chimp orthologous proteins are identical is inversely proportional to protein length, this estimate will be a little high. Let us imagine, conservatively, that the average of 2 amino acids differing per protein was consistent across all proteins, not just the longest 71% of them. This would mean that the probability that two orthologous amino acids are identical is equal to (998/1000) or 99.8%.

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You guys and your probability arguments...ok...you were saying...

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So the average probability of identity for single amino acids is close to 100% and over 99.5%, whichever way you look at it. NOT 29%!!!

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Look at the quote and we can take this up when you realize what I am talking about.

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Finally, there is your assertion that the natural mutation rate cannot account for the number of differences between chimp and human genomes. Let's say that the generation length for humans, chimps and their proto-species is around 15-20 years. Over the six million years since divergence, that gives us 300,000 to 400,000 generations per lineage. Since there are two lineages that can accumulate mutations, we have a total of 600,000 to 800,000 fertilization events separating a modern chimp from a modern human. Given that the nature paper declared 40 million mutation events, that gives us 50-66 mutations fixed per POPULATION per generation.

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Finally something at least reasonably cognizant. The high end would be 7 million years but most molecular clocks would put it under 5 mya. Prior to 2 1/2 million years ago your imaginary human ancestors stood three foot tall, had the cranial capacity of a chimpanzee and wre for all intents and purposes knuckle dragging apes. The first truely human looking hominid was Turkana Boy who stood 6 foot tall with a cranial capacity of 900 cc at adulthood which puts him well within the human range.Nevertheless, the outer limit for the chimpanzee/human split is 7 million years. That is 350,000 generations with the mutation rate at...let's see...2 x 10^-8 per diploid generation. That's 2 per 1oo,ooo,ooo nucleotides copied. The human genome is 2.85 billion nucleotides long but lets round it off to 3 billion. That is 60 per duplication and there are two geneomes, one from each of the parents. That comes to 120 per generation and believe me that is a rough estimate.This is the point, that is not the 200 nucleotides that would have had to be fixed in 350,000 generations. Mind you these mutations our ape cousins are experiencing are germline mutations which makes them inheritable, not nessacarily fixed.

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The number of new mutations arising per individual is around 100. If we were to assume a mean historical effective population size of around 25,000 for each proto-species (consistent with chimpanzee demographic data), the observed divergence between chimps and humans requires something of the order of 2-3 mutations to be fixed for each 100,000 mutations occuring. That doesn't seem unreasonable by any means.

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The protein coding genes account for roughly 1% of the human genome. That would make it 300 Mb and you are wanting 1 or 2 mutations fixed. You are obviously talking about amino acid substitutions so you should take into consideration the deleterious effects. Don't worry about calculating this the paper has allready done that for you:"Under the assumption that synonymous mutations are selectively neutral, the results imply that 77% of amino acid alterations in hominid genes are sufficiently deleterious as to be eliminated by natural selection. Because synonymous mutations are not entirely neutral (see below), the actual proportion of amino acid alterations with deleterious consequences may be higher. Consistent with previous studies8, we find that KA/KS of human polymorphisms with frequencies up to 15% is significantly higher than that of human-chimpanzee differences and more common polymorphisms (Table 3), implying that at least 25% of the deleterious amino acid alterations may often attain readily detectable frequencies and thus contribute significantly to the human genetic load."Well over 80% of mutations do nothing at all and the vast majority of the balance are deleterious. There is a rare beneficial effect, especially in highly conserved regions like the brain. So you have 100-120 bp worth of mutations. Of those 1-2 are in the actual genes, of those 3 out of 4 are going to be delerious enough to be acted upon by natural selection. That means you will need at least 4 per per diploid generation.This is the thing, the Human Genome Project has found millions of these little buggers and do you want to know what the effects are? You allready know, in the event that you don't I can provide you with an extensive list from the Human Genome Project I can even tell you how to get a free poster with them listed.Interested in a free poster from HGP?

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Summary:

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Probability that two orthologous amino acids are identical = 99.8%
Probability that two orthologous nucleotides are identical = 96%
Probability that two orthologous proteins are identical = 29%

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I'm just curious at this point since there is not a snowballs chance in Bagdad that this is an accurate statement. Do you usually get by with this kind of a jacked up misrepresentation of scientific literature?Have a nice day.
eggasaiEdited by eggasai, : transcript errorsEdited by eggasai, : No reason given.

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No. A single coding nucleotide sequence always has at least one reading frame.

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Don't you get tired of being wrong? Nonesense, there is no such thing as a coding nucleotide. There are aminio acid seqeunces in protein coding gene have to translate into meaningfull proteins. If the chain is broken a stop codon will be inserted shutting down the reading frame. There is no actual frame, it's just an expression and if you are going to be making this kind of a fundamental mistake I'm going to have some fun with this.

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Whether fixed mutations are deleterious or not makes no difference to the proportion of observed differences between the two genomes. We don't even need to know the function of the genes that differ, just the number of nucleotides. I must say that your entire discussion of selection against deleterious mutation seems irrelevant when we are discussing fixed mutations.

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Whether they are deleterious or not is the key factor in whether or not they are fixed. Three out of four will be deleterious enough for there to be negative selection. That means that most of the mutations that pop up on the NS radar get zapped. Deleterious mutations do get fixed and the result is disease, disorder and death.Fundamental error #2, you don't realize the roles of deleterious effects on fixation.

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No. First, amino acids are not translated into proteins. More substantively, you have to read more carefully:

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No, first of all you need to learn basic biology before you start pontificating about how things work:

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They are saying that 29% of the proteins do NOT differ at any amino acid positions. The remaining proteins, which DO differ, differ by an average of only two amino acids. This is a surprisingly high level of similarity, not a low level.

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That's the first thing you got right and you didn't correct what I said, you finally understood something fundamental. Most of the protein coding gene differ by one amino acid sequence in each of the two genomes. That's a mean average with some diverging by a more.

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(in edit - I also need to read more carefully - the sentence is properly understood as saying that the median number of amino acid differences is two, including 29% of proteins with zero differences. An overall mean of 2 was used in my previous posts)

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Those mutations that you are putting in the protein coding genes are probably deleterious and could shut the reading frame down. You don't seem to have a grasp of this fact so I will continue to repeat it until you do.

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Sure, I ignored chromosomal rearrangements since there are only nine of them. Compared to the 40 million substitution or indel mutations they are negligible in terms of the mutation rate calculations. Repeat my analysis with "forty-million and nine" mutations instead of "forty million mutations" and there should be little consequence.

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The ones described in the paper are only the major ones, there are a lot of others. These are 2 Mb to 4 Mb in length for 20 Mb and they don't interest you even though we are talking about half as many base pairs involved as the single nucleotide substitutions.

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You think three nucleotides have to mutate in order to change a single amino acid? You are wrong.

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No, I don't think that nor have I said anything of the sort. It could be a single nucleotide in each of the amino acid seqeunces but if it's just one nucleotide you are limited to what kind of an amino acid sequence it involved. Like I keep telling you a single nucleotide can shut the reading frame down making the gene inoperative. Your not getting that but it's not my fault you didn't learn basic biology before you started preaching it.

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Hmmmn.... Hard to grasp what you are getting at, but you seem to think that only 20 possible codons are valid? This might explain why you think random mutation is such a non-starter. But if that's what you think, you are wrong. In the standard genetic code there are sixty-four possible codons (that is 4^3, not 4^4 as you claim) and arond 61 of them code for valid amino acids, the remainder for stop codons.

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You are right about the sixty-four possible codons, it is 4^3=64, I was all set to compliment you on getting something right. There are 20 amino acids of life not 61, notice the three stop codons you were trying to factor in on the chart: Codons don't code for anything, triplet codons are formed together in amino acid seqeucnes, the amino acid seqeunces are translated into proteins. You are defending your sacred evolution from creationist infidels and you don't know the central dogma of biology!?I'll give you a hint, DNA-transcription-RNA-translation. Artemis will not be pleased with you if you don't learn the central dogma. Edited by eggasai, : transcription errors

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This is just complete nonsense. Where did you come up with such a ludicrous 'fact'. Take a look at the genetic code, this figure uses the RNA codons so for the DNA counterparts substitute Ts for Us.

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You guys like to exaggerate pedantic points don't you? Your buddy had one fundamental error after another but that's ok, he's an evolutionist. Anyway, when we have trudged through the pedantic biology sermons maybe you guys would like to get back on topic. You might want to clue your buddy in on the terminiology and actually read some of the literature before we start.The thread is about the genetic basis for this giant leap of evolution: I'm glad you are so well versed in basic biology, your going to need it. Edited by eggasai, : transcript errorsEdited by AdminJar, : No reason given.Edited by eggasai, : Checking out what the Mod did.

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It would be nice to go on to discuss the evolution of brain-related genes, as you suggest, but I don't see how it can be constructive if you misunderstand the most basic elements of molecular biology (notwithstanding your hubristic attacks on the understanding of others).

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I noticed that you are not as hypercritical about mistakes when it's one of your own. I just wonder how many creationists you have poisoned the well for, but no matter. Rest assured that the deleterious affects of mutations on neural genes is going to be discussed.

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How can you write that, directly after providing a figure showing precisely the opposite?

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Because they don't unless they come in triplet codons. Your boy Mick said that each nucleotide had at least one reading frame. I didn't see you go into spasms over that, I expect this is just a diversionary tactic while you try to get a handle on the Chimpanzee Genome paper.

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Codons "code for" amino acids. A triplet of nucleotides (i.e. a codon) within the DNA sequence or within the transcribed RNA sequence directly corresponds to a single amino acid within the protein. That correspondence is called "coding".

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No they don't, amino acids code for proteins, nucleotides are just the basic element of precise amino acid sequences. I'm neither baffled nor dazzled by how you conflate that basic biology and try to magnify percieved errors. I've done this before and I know what happens when you guys are confronted with the evidence.

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Amino acid sequences are not made out of codons, nor are codons "formed" in amino acid sequence. An amino acid sequence is just that - a series of amino acids. There are no nucleotides or codons within an amino acid sequence.

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You preach fundamentalist biology to me and make an assinine remark like that? Amino acids are composed of triplet codons which are three nucleotides called triplet codons, it just an expression really. Watson and Crick determined that codons were triplet by removing 1 or two of the nucleotides. This became the 'central dogma' of biology (DNA-trascription-RNA-translation) in their famous paper on the subject.

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No, the amino acid sequence IS the protein.

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No it's not, the amino acid sequence is translated into proteins in the ribosome...jezzz...talk about a fundamental error.

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I'm sorry to keep pressing on these basic matters but I don't see how it will be possible to discuss mutation rates in protein-coding genes involved in the brain without agreement on these matters.

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I don't either, you guys need basic biology. At this point diving into the scientific literature would be worse then useless. If you learned something about comparitive genomics now you would probably learn it wrong. We can spend some time on the Biology primer, it's better then trying to explain everything about the papers we are going to be looking at.

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This is really just the result of your not understanding transcription and tranlsation. But your view that two out of three nonsynonymous mutations result in an inviable protein (presuming that a protein "not containing the amino acids of life" is inviable) is going to seriously cloud your judgement of the likelihood of mutations being fixed in brain-related genes.

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I'm glad you brought that up, you guys have no clue what a deleterious effect from a mutation is either. Why don't you forget about the synonomous/nonsynonomous ratio right now, you aren't even congnizant of it's relevance or signifigance. You need to learn what happens when a mutation happens in the amino acid seqeunce: So why don't you elaborate on the 'central dogma' of biology?You can't continue into comparitive genomics untill you get some basic terminology down and at least a rudimentary understanding of the principles.

This is almost cliche, evolutionists love to cut and paste those skulls and let the illusion of gradual transition sink in. This is what the thread will be about, this is Homo habilis who stood 3 foot tall with the cranial capacity of an ape: In 2 1/2 million years the cranial capacity had not signifigantly diverged from that of apes. The above skull is not much bigger then an apes,Then in less roughly 300 ka Turkana Boy appears suddenly along with the Homo erectus fossils. Edited by eggasai, : Had to cut the lesson short

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I though amino acids make up the basic components of proteins and not code for them.

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Originally I said that a single nucleotide substitution in the protein coding genes could shut down the reading frame. The rest of it is a tangent, this is how the amino acid sequence codes for proteins: The triplet codons make the amino acids. The amino acids in a specific sequence make up the 'code'. My point was that there was no such thing as a coding nucleotide, it's the amino acid seqeunce that determines the protein. Apparently, things are going to be bogged down on semanitcs and basic biology for a while. I was trying to talk about the protein coding genes but instead we are spending all our time on what a protien code is.They think I don't know basic biology, that's the real problem. Edited by eggasai, : transcript errors

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Several individuals are trying to do you a favour and point out where you lack knowledge of some basic biology. Do NOT get nasty about it or a suspension will follow.

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No problem, I'm actually enjoying the basic biology primer.

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You should bear in mind that brain size is correlated with body size. For this reason, absolute brain volumes are not a very useful comparative measure; rather we would normally want to use a relative measure of brain size which takes into account differences in overall body size. Because when the whole body gets larger, the brain gets larger as well but doesn't necessarily imply evolutionary change specific to the brain.

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Still the cranial capacity becomes central to the definition Hominids based on the cerebral rubicon. Cranial capacity is the most distictive feature of the genus Homo, the various definitions within that genus reflect this basic concept.

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If you take body size into account, it seems to me at least that to have the same size brain as an ape when you are only three feet tall is having a LARGE brain size, not a small one, since apes are aready considered fairly large-brained and they can grow up to six feet.

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Gorillas stand pretty tall but their cranial capacity still isn't as big as a chimpanzees, who stand about 3 foot tall. The cerbreal rubicon has long been that main morphological traits that distinquishes hominids from apes. It has become increasingly clear to me that the not all of the hominids belong in the genus Homo. Cranial capacity still marks a clear line of demarkation.

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If you calculate values for the various primates from fossils and extant species, and take the average EQ, you get the following values (mean from both sexes)

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Dimomorphic variance also translates into cranial capacity differences. Hablines generally range from 510cc to 775cc and besides bipedal frames they are clearly knuckle dragging apes.

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I think this data clearly shows that it is wrong to suggest, on the basis of absolute brain size in Homo habilis versus ape that no trend towards larger brains was present in the early members of the Homo genus.

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The trend in the early hominids suggests to me that the trend in ape lineages was a decrease in absolute brain size. Every ape skull dug up in Africa from prehistory is automatically put in human lineage. There should be a concerted effort to determine ape lineage but the need for transitionals takes preferance.

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If you look at these encephalizatoin quotients across time, you see a major jump in the Australopithecines, where go from an average kind of brain size to one that is twice as large as expected; then a steady, gradual increase within the Homo genus; followed by a second major jump in the early Homo sapiens, where we go from a species with a brain 3.9 times larger than we would expect based on body size, to a species with a brain 5.3 times larger than we would expect.

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What we really have for the Austropithecenes is fragmentary peicemeal compositions. There is no genuine absolute brain/body size ratios. With the habilines they are well below the cranial capacity for humans and in some cases for the Homo genus. What you are looking at in ape lineages is a decrease in cranial capacity and a loss of bepediality. That's why this gets so convoluted, too often they are automatically considered human ancestors rather then ape.

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If you look at these encephalizatoin quotients across time, you see a major jump in the Australopithecines, where go from an average kind of brain size to one that is twice as large as expected; then a steady, gradual increase within the Homo genus; followed by a second major jump in the early Homo sapiens, where we go from a species with a brain 3.9 times larger than we would expect based on body size, to a species with a brain 5.3 times larger than we would expect.

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The austrophithecines average slightly above that of a modern ape. The overall brain size did not double from the Austropithecines to the habilines. Homo habilis had a cranial capacity below 600cc while the austropithecines has a cranial capacity about 400cc. The cranial capacity does not actually make a signifigant jump until Homo habilis where it goes from under 600cc to close to 1000cc.What needs to be understood is that the austropithecines and hablines are actually a mixture of gorilla and chimpanzee ancestors. The human ancestors are actually the Homo erectus fossils.

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You prove them right when you say things as ignorant as "amino acid sequence codes for proteins".

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The amino acid seqeunce is the code the proteins are translated from in the ribosome.

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I mean you can't even seem to read your diagram right. That sequence of amino acids down there at the bottom? That's the protein. I mean it's even labeled "growing protein chain."

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I don't know what you think the problem is here but amino acids are translated into proteins. The amino acids determine the protien chain but they have to be translated into proteins, that is about as basic as it gets.

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No, they don't. They specify amino acids, via the mechanism of tRNA. Amino acids are produced at other places in the cell, or aren't produced at all - they're provided by the diet of the organism. (That's why there's 9 essential amino acids that, as a human, you're required to injest from food. Your cells are unable to produce them de novo.)

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Yes they do, the amino acid is defined by the triplet codons, remove a condon and you got nucletides.

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No. The nucleotides (A,G,C,T) make up the code. The amino acids they code for make up the protein. Amino acids are the fundamental structural units of proteins, when they're joined together (amine to carboxyl) with peptide bonds. Folding polypeptide chains produce the spacially-determined active sites that allow proteins to catalyze chemistry within the cell.

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No, the nucleotides make the triplet codons of the amino acids. Nucletides don't code anything in and of themselves and your spliting semantical hairs. This is twice you tried to contradict me and then elaborated from there on a tangent.

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Until your misunderstandings are corrected, debate is impossible. We can't have a debate with you until you know what you're talking about. No, no thanks are necessary - it's our pleasure to educate you.

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That's kind of funny, most of the basic biology we are discussing could be covered in one post. I don't know if conflating the basic biology is just a rethorical tactic or you actually believe what your saying.This all started with the misconception that a nucleotide has some intrinsic coding quality. I mentioned in passing that a single nucleotide substitution could get the reading frame shut down. I was contradicted and told that every coding nucleotide has at least one reading frame. Terms like; reading frame, coding sequence and protein sequence are just expressions. The basic principle was summed up as DNA-transcription-RNA-translation (aka the central dogma of biology)A debate is impossible because no one seem cognizant of this ubiquitious principle in biology. Basic errors are actually being made not because of my misunderstanding but an attempt to correct and contradict me.The original point was that the protein coding genes show differences at an amino acid sequence level. One regulatory gene 118 nucleotides long has diverges from chimpanzees by 18 nucleotides. The same regulatory gene when comparing chimps to chickens has 2 substitutions which represents 310 million years. When this point couldn't be answered the discusssion was derailed with this...basic biology debate.Edited by eggasai, : transcript errors having a deleterious affect in the alphanumeric word codeing sequences. You know...typos.