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Author Topic:   Genetics and Human Brain Evolution
eggasai
Inactive Member


Message 76 of 157 (360090)
10-31-2006 10:24 AM
Reply to: Message 72 by Dr Adequate
10-30-2006 10:25 PM


Re: Eggasai is producing mashups of his previous posts.
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.
This message is a reply to:
 Message 72 by Dr Adequate, posted 10-30-2006 10:25 PM Dr Adequate has not yet responded

  
sfs
Member (Idle past 788 days)
Posts: 464
From: Cambridge, MA USA
Joined: 08-27-2003


Message 77 of 157 (360099)
10-31-2006 11:09 AM
Reply to: Message 71 by eggasai
10-30-2006 9:47 PM


Re: Getting the numbers right
quote:
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.

And I very much doubt that taking a good look at the chimpanzee genome paper will do any good. Assuming you're Mark Kennedy, and not merely someone copying his arguments and his prose style, then we've already been through the chimpanzee genome paper at great length over on Christian Forums, and you're still making the same mistakes about it.

Regardless of whether you're Mark or not, you're making numerous mistakes. Probably the most important one is trying to compare the mutation rate (as measured in modern humans) for single-base substitutions with the total number of bases mutated (from all kinds of mutation) in the comparison of humans and chimpanzees. You can't compare the rate of mutation events with the total number of bases changed in mutations, at least not if you want to do anything sane.


This message is a reply to:
 Message 71 by eggasai, posted 10-30-2006 9:47 PM eggasai has responded

Replies to this message:
 Message 78 by jar, posted 10-31-2006 11:21 AM sfs has not yet responded
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jar
Member
Posts: 31262
From: Texas!!
Joined: 04-20-2004
Member Rating: 2.8


Message 78 of 157 (360101)
10-31-2006 11:21 AM
Reply to: Message 77 by sfs
10-31-2006 11:09 AM


Re: Getting the numbers right
The subject was also discussed at Cross+Flame and all the same errors are being repeated here. Folk are free to continue responding but should understand that the final outcome will simply be the initial starting point.


Aslan is not a Tame Lion
This message is a reply to:
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eggasai
Inactive Member


Message 79 of 157 (360125)
10-31-2006 12:41 PM
Reply to: Message 73 by Wounded King
10-31-2006 2:50 AM


Re: I've read the papers, now why not address the isssues I raised?
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.

So you respond with this little quip...

quote:
Now why would I do that? Oh right, its beacuse you just said ...

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:
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.

That's exactly right and your problem would be...?

quote:
So in fact if ayone is making the confusion you just accused me of it was in fact you. You only just claimed in the previous post that all of those gross structural changes were in frame indels, do you see where I might have got the idea that that was what you thought?

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 were talking about HAR1 again suddenly were you, OK. Why should anyone expect to see in frame indels in a non-coding region of a gene? I have been making this point repeatedly and you have yet to address it. The 118 nucleotide sequence does not functionally code for any amino acids, if anything its function appears to be mediated by the secondary structure of the resulting RNA transcript.

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'm not sure why you thought the reference was vague given that you were talking specifically about the chromosome 22 paper in the post I was replying to. I appreciate that you are having to keep track of a number of seperate conversations at once but it isn't hard back to trackback in these threads.

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:
20 whats now? Is it nucleotides or mutations today? If it is mutations then as has been pointed out the figure is wrong. If it is nucleotides then, as has also been pointed out repeatedly, you are failing to take into account the many large scale mutations which can account for hundreds to millions of bases in one event.

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:
OK, for someone so keen to talk about how great his references are this is the sort of figure which could do with some evidentiary backing and also some rationale for why it makes any difference whatever to the matter under discussion. What is your evidence that anything has stopped or the the modern mutation rate has leveled off from something. I've seen similar rates quoted in some papers (Kondrashov, 2003) but it would help to know exactly what you are basing your figures on since they report similar rates estimated from the comparison of chimp and human pseudogenes. That paper itself estimates 'that the total number of new mutations per diploid human genome per generation is ~100'. Why do you consider these numbers insufficient?

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:
The costs are enormous, but I think there is clearly a case to be made that the substantial quantitative, if not qualitative, increases in our mental activities has had a clear positive effect on our ability to survive so the benefits may have been sufficienty greater than the costs. I don't see in the slightest how this conflicts with any evolutionary biology in an anagenetic model or otherwise.

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


This message is a reply to:
 Message 73 by Wounded King, posted 10-31-2006 2:50 AM Wounded King has responded

Replies to this message:
 Message 80 by kuresu, posted 10-31-2006 12:48 PM eggasai has responded
 Message 83 by sfs, posted 10-31-2006 2:08 PM eggasai has responded
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kuresu
Member (Idle past 768 days)
Posts: 2544
From: boulder, colorado
Joined: 03-24-2006


Message 80 of 157 (360129)
10-31-2006 12:48 PM
Reply to: Message 79 by eggasai
10-31-2006 12:41 PM


Re: I've read the papers, now why not address the isssues I raised?
I know what the problem is, you don't know what a reading frame is

you don't know who WK is, do you?
he's a geneticist, a real live, honest to god, working scientist.
and you don't get to those positions by being stupid.

now tell me, what's you're qualification in genetics?


Want to help give back to the world community? Did you know that your computer can help? Join the newest TeamEvC Climate Modelling to help improve climate predictions for a better tomorrow.
This message is a reply to:
 Message 79 by eggasai, posted 10-31-2006 12:41 PM eggasai has responded

Replies to this message:
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eggasai
Inactive Member


Message 81 of 157 (360147)
10-31-2006 1:54 PM
Reply to: Message 77 by sfs
10-31-2006 11:09 AM


Re: Getting the numbers right
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:
And I very much doubt that taking a good look at the chimpanzee genome paper will do any good. Assuming you're Mark Kennedy, and not merely someone copying his arguments and his prose style, then we've already been through the chimpanzee genome paper at great length over on Christian Forums, and you're still making the same mistakes about it.

Like counting all of the base pairs in the indels and applying them to the mutation rate as measured in base pairs.

quote:
Regardless of whether you're Mark or not, you're making numerous mistakes. Probably the most important one is trying to compare the mutation rate (as measured in modern humans) for single-base substitutions with the total number of bases mutated (from all kinds of mutation) in the comparison of humans and chimpanzees. You can't compare the rate of mutation events with the total number of bases changed in mutations, at least not if you want to do anything sane.

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.


This message is a reply to:
 Message 77 by sfs, posted 10-31-2006 11:09 AM sfs has responded

Replies to this message:
 Message 85 by sfs, posted 10-31-2006 2:28 PM eggasai has responded

  
eggasai
Inactive Member


Message 82 of 157 (360149)
10-31-2006 2:05 PM
Reply to: Message 80 by kuresu
10-31-2006 12:48 PM


Re: I've read the papers, now why not address the isssues I raised?
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."

http://en.wikipedia.org/wiki/Open_reading_frame

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.


This message is a reply to:
 Message 80 by kuresu, posted 10-31-2006 12:48 PM kuresu has not yet responded

  
sfs
Member (Idle past 788 days)
Posts: 464
From: Cambridge, MA USA
Joined: 08-27-2003


Message 83 of 157 (360150)
10-31-2006 2:08 PM
Reply to: Message 79 by eggasai
10-31-2006 12:41 PM


Re: I've read the papers, now why not address the isssues I raised?
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.

He doesn't realize it because it isn't true. The regulatory gene in question, HAR1, does not code for any amino acids -- it's an RNA gene that is never translated into protein. (And a sequence of amino acids does not code for a protein; a sequence of (bonded) amino acids is a protein.)
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.

Base pairs are pairs of nucleotides. What are you talking about here?
quote:

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?

I have no idea what this question is supposed to mean.
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.

No, it would not require 20 mutations per year; it would require 20 mutated nucleotides (including indels) per year. Those 20 mutated nucleotides occur in ~5 mutations per year. (And that's including mutations in both chimps and humans.)
quote:

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?

I don't know about anyone else, but I certainly think it's no big deal
This message is a reply to:
 Message 79 by eggasai, posted 10-31-2006 12:41 PM eggasai has responded

Replies to this message:
 Message 87 by eggasai, posted 10-31-2006 3:10 PM sfs has responded

    
Dr Adequate
Member
Posts: 16099
Joined: 07-20-2006


Message 84 of 157 (360155)
10-31-2006 2:25 PM
Reply to: Message 78 by jar
10-31-2006 11:21 AM


Re: Getting the numbers right
The subject was also discussed at Cross+Flame and all the same errors are being repeated here. Folk are free to continue responding but should understand that the final outcome will simply be the initial starting point.

You mean to tell us that he's been shooting this line for a year or more, and he's still coming out with stuff like this:

it was concluded we descended from apes before biology was even a seperate discipline in science

and this:

Biological evolution makes assumptions and then makes homology arguments from any simularity.

and this:

mutations affecting neural genes are exclusivly deleterious

and this:

Relaxed functional constraint would be deadly

and this:

The point is that 4 mya the cranial capacity was just over 400cc and remained static until about 2 mya.

and this:

The first step is deconstructing Darwinism and genetics is doing a fine job of that on it's own.

and this:

makes sense that certain genes are going to be different but not in genes involved in the brain or liver. However, it is exactly here that you see the spectacular mutations. Sure, 40,000 amino acids don't seem like a whole lot until you take into consideration that this is 120,000 nucleotides at the very least. Not only do they have to be substituted in triplet codons but fold into meaningfull proteins.

and this:

Major mophological adaptations in a relativly brief period of time. This is exactly what a creationist would expect

and this:

The Human Genome Project has a website with educational material on DNA and how it works. Not once is evolution even mentioned.

and this:

Turkana Boys cranium has been compared to modern Chinese and it is only slightly smaller and as far as then can tell to internal proportions are pretty close.

and this:

Projecting into the prehistoric and primordial past is well beyond the purview of science

and this:

natural selection is not a big contributor to human evolution

and this:

What you really are trying to hide is the fact that your presumption of a single common ancestor has nothing to do with the actual science. Biology does not need the single common ancestor model. Mind you, I'm not saying that there are no common ancestors (plural), just that your insistance on a single common ancestor is pure undiluted mythology.

and this:

Then the amino acid seqeunces are translated into proteins

and this:

4^4 is 64

and this:

The chances of an amino acid seqeunce turning into one of the amino acids of life is less then one in three.

and this:

Codons don't code for anything, triplet codons are formed together in amino acid seqeucnes, the amino acid seqeunces are translated into proteins.

and this:

amino acids code for proteins, nucleotides are just the basic element of precise amino acid sequences.

and this:

the amino acid sequence is translated into proteins in the ribosome

and this:

Watson and Crick determined that codons were triplet by removing 1 or two of the nucleotides.

and this:

The amino acids in a specific sequence make up the 'code'. My point was that there was no such thing as a coding nucleotide

and this:

The trend in the early hominids suggests to me that the trend in ape lineages was a decrease in absolute brain size.

and this:

Every ape skull dug up in Africa from prehistory is automatically put in human lineage.

and this:

remove a condon and you got nucletides

and this:

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.

and this:

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.

and this:

Darwin's On the Origin of Species is just one long arguement against 'special creation'.

and this:

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.

and this:

Cranial capacity represents a cerebral rubicon that marks a clear line of demarkation in the transition from ape to humans.

and this:

The only reason that the mutation rate is not 0 is because of the physiological costs of adaptation.

and this:

a reading frame is just the the amino acid sequence

Good grief.

This isn't an argument, it's a collection of idées fixes.


This message is a reply to:
 Message 78 by jar, posted 10-31-2006 11:21 AM jar has not yet responded

Replies to this message:
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sfs
Member (Idle past 788 days)
Posts: 464
From: Cambridge, MA USA
Joined: 08-27-2003


Message 85 of 157 (360158)
10-31-2006 2:28 PM
Reply to: Message 81 by eggasai
10-31-2006 1:54 PM


Re: Getting the numbers right
quote:
Like counting all of the base pairs in the indels and applying them to the mutation rate as measured in base pairs.

No, like counting all the base pairs in the indels and applying them to the mutation rate as measured in mutation events, which is what you've just done here. The 2x10^-8/bp/generation is the number of mutation events, not the number of base pairs. (It's also just the single-base substitution rate, but that's less important.) It doesn't matter how many times you make that comparison: it will be wrong every time you do.

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.

No, it's not insane to measure a mutation by the number of base pairs. It would be a fine thing to do, if we had any way of doing it for current human mutations. We don't. That's why we make comparisons using the mutation rates that we actually have measured, like the single-base substitution rate.

If you want to compare the total human/chimp divergence in base pairs against the measured rate at which base pairs change by mutation in humans, that's a perfectly sensible thing to do. To do it, however, you're first going to have to go out and measure that second number, because no one else has done it yet. Good luck with that.

quote:
The average indel is something like 300 bps,


Where did you get that number? The numbers you love to quote from the chimp genome paper give 5 million indels, totaling ~90 million bp. That's 18 bp per indel, not 300.

quote:

your trying to tell me that every generation there was at least one fixed along with 5 single nucleotide substitutions.


No, I'm trying to tell you that every generation there were ~50 single nucleotide substitutions fixing and 7 indels fixing.
quote:
I'm pretty much convinced that the only mistake I'm making is introducing myself as a creationist.

You may be convinced of that, but in reality you've made numerous errors in basic biology and genetics.
This message is a reply to:
 Message 81 by eggasai, posted 10-31-2006 1:54 PM eggasai has responded

Replies to this message:
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sfs
Member (Idle past 788 days)
Posts: 464
From: Cambridge, MA USA
Joined: 08-27-2003


Message 86 of 157 (360163)
10-31-2006 2:36 PM
Reply to: Message 84 by Dr Adequate
10-31-2006 2:25 PM


Re: Getting the numbers right
quote:
You mean to tell us that he's been shooting this line for a year or more, and he's still coming out with stuff like this

It's been going on for a couple of years on Christian Forums, with hundreds of posts replying to him.
quote:
Good grief.

This isn't an argument, it's a collection of idées fixes.



Well, yes. The sad thing is that he's still more interesting that 99% (at least) of creationists.
This message is a reply to:
 Message 84 by Dr Adequate, posted 10-31-2006 2:25 PM Dr Adequate has not yet responded

    
eggasai
Inactive Member


Message 87 of 157 (360172)
10-31-2006 3:10 PM
Reply to: Message 83 by sfs
10-31-2006 2:08 PM


Re: I've read the papers, now why not address the isssues I raised?
quote:
He doesn't realize it because it isn't true. The regulatory gene in question, HAR1, does not code for any amino acids -- it's an RNA gene that is never translated into protein. (And a sequence of amino acids does not code for a protein; a sequence of (bonded) amino acids is a protein.)

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:
Base pairs are pairs of nucleotides. What are you talking about here?

Just what I said, single nucleotide substitutions and indels measured in base pairs.

quote:
I have no idea what this question is supposed to mean.

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:
No, it would not require 20 mutations per year; it would require 20 mutated nucleotides (including indels) per year. Those 20 mutated nucleotides occur in ~5 mutations per year. (And that's including mutations in both chimps and humans.)

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 don't know about anyone else, but I certainly think it's no big deal

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.


This message is a reply to:
 Message 83 by sfs, posted 10-31-2006 2:08 PM sfs has responded

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sfs
Member (Idle past 788 days)
Posts: 464
From: Cambridge, MA USA
Joined: 08-27-2003


Message 88 of 157 (360179)
10-31-2006 3:51 PM
Reply to: Message 87 by eggasai
10-31-2006 3:10 PM


Re: I've read the papers, now why not address the isssues I raised?
quote:
Ok, so the triplet codons in regulatory genes don't code for amino acids.

It would be nice if you could accurately paraphrase even one thing you're responding to. I said that the this regulatory gene does not code for any amino acids. I didn't say anything about regulatory genes in general.
quote:
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.



My reaction was, "Wow, that's a lot of substitutions." Then I thought about it for a minute and realized that this was the most extreme case in the genome, and the most extreme case of anything in the genome is likely to be rather, well, extreme. And then I remembered that the extreme case among protein-coding genes had (if I remember correctly) fourteen amino-acid differences between humans and chimpanzees, and I didn't find it all that surprising. Impressive, yes, but not really surprising.

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?

You need to clarify your clarification, because that isn't even English. Do you mean do I have more base pairs that have changed within the last generation because of indels than because of single-base substitutions? If that's your question, then I don't know the answer, since it depends on the individual. On average, the number of base pairs changed by indels is larger than the number changed by substitutions, but for most individuals the number is probably smaller. That's because the rarer large deletions skew the average.

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?


No, I have about 100 substitutions and about 14 indels. That works out to about 5 or 6 per year. (Generations are longer than years.) And indels still aren't 300+ bp long (on average).

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.

And what mutation rates might these be that you're looking at? Where did you get them from? The only mutation rates based on modern human populations that include indels that I've seen are hopelessly biased against observing long indels.

quote:
I am also suspect that the accumulated single nucleotide substitutions outweigh indels in length as measured in base pairs.

Your suspicions don't count for anything.

quote:
Finally, I think most, if not virtually all the transcript errors in the germline cells are repairable in successive generations.

Transcript errors aren't mutations. This is one of the basic biology mistakes you keep making.

quote:

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.

Great. Combine your assertion with some evidence, and you'll have . . . some evidence.
This message is a reply to:
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Wounded King
Member (Idle past 2349 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 89 of 157 (360199)
10-31-2006 5:27 PM
Reply to: Message 79 by eggasai
10-31-2006 12:41 PM


A little exercise for thy cerebellum's sake.
I know Sfs has already addressed a lot of this so please forgive any duplications of the covered material.

I know what the problem is, you don't know what a reading frame is.

I'm not sure why you think open reading frames are particularly important in this instance, but rest assured I know what one is.

a gross stuctural change is nothing more then 20% of the protein coding genes are much more different then predicted.

This is not the case. The 'gross structural change' refers to the actual change to the sequence. My point against this was that not all of the 'gross structural changes' were indels as you contended, your point seems to have been that you don't know what the hell you are talking about.

From the paper...

47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms.

So there are significant structural changes within the genes affecting their products. These are the gross structural changes in 20.3% of the genes. It is not that 20.3% being unexpectedly divergent is in itself a gross structural change, of these gross structural changes only 15 are indels.

You don't realize that the regulatory genes come in amino acid sequences do you?

There are lots of different types of regulatory gene, the vast majority with which we are familiar are indeed protein coding but there is a rapidly growing body of evidence to show that there are several other forms of genetic regulation which are mediated by non-coding RNA transcripts, one such form are microRNAs such as have been just detailed in terms of the differences betwen chimps and human with regard to the brain (Berezikov et al., 2006).

Now as far as mutations that involve in hundreds of millions of base pairs or nucleotides then I want to see it.

Reading comprehension really isn't your strong suit is it, what I said was 'hundreds to millions' and you yourself pointed out at least one 4Mb chromosome rearrangement.

Oh really? Here is a list of known effects from mutations that involve genes in the human neural system

Which is exactly what I predicted you would produce ad far back as the first page, and as I pointed out then the existence of some deleteious mutations with phenotypic effects significant enough to be readily apparent in no way means that all mutations will be detrimentla, I see that you have even backpedalled a bit and are now only saying that mutations would be detrimental most of the time. The seems to be an equally unevidenced assertion but a considerable improvement since it at least allows for some mutation, not every single one being lethal as you previously claimed.

I'd now like to revisit Har1. Lets forget about the paper for a moment and look at the data.

This link will take you to the entrez nucleotide page for the Har1 sequences from the paper we were discussing. You will note that both sequences are identified as 'non-protein-coding RNA'.

If we click on the second sequence there Har1A then you will be taken to the sequence of the highly accelerated region.

If you scroll down to just before the actual sequence starts you will find a 'misc feature' annotation link which is the actual 'highly conserved' 118bp sequence.

If you copy that sequence and put it into Entrez's ORF finder program it won't find a single one. If you take the whole Har1 region and put it through ORF finder you will see a number of possible ORF's and the nucleotide ranges they span, none of these ORFs span the region from 851-968 within which the highly conserved region is found.

If there is a mistake here then please show me where it is, if not then please finally admit that this sequence does not functionally code for any protein sequence whatsoever!!

This exercise shouldn't take more than a couple of minutes at most so please go through it and tell me what you are seeing that neither I, the ORF-finder program nor the authors of the original paper can see.

TTFN,

WK

Edited by Wounded King, : No reason given.


This message is a reply to:
 Message 79 by eggasai, posted 10-31-2006 12:41 PM eggasai has not yet responded

    
eggasai
Inactive Member


Message 90 of 157 (360200)
10-31-2006 5:29 PM
Reply to: Message 85 by sfs
10-31-2006 2:28 PM


Re: Getting the numbers right
quote:
2x10^-8/bp/generation,is the number of mutation events, not the number of base pairs

Then what does bp stand for in your formula if not base pairs?

quote:
No, it's not insane to measure a mutation by the number of base pairs. It would be a fine thing to do, if we had any way of doing it for current human mutations. We don't. That's why we make comparisons using the mutation rates that we actually have measured, like the single-base substitution rate.

I'll buy we don't know, we can't tell, its out of reach for for technology and knowledge. What I don't buy is the constant unsubstantiated assertion that genetics and single common ancesotry blends together in dovetail fashion.

Do you think I took an interest in this whole subject because I am fascinated with biogenomics or I like being talked to like I'm mentally deficient. The one thing that has fascintaed me about all of this is the intensity everyone from a freshman Biology 101 student to a PHD has in common is that they find creationism detestable.

quote:
Where did you get that number? The numbers you love to quote from the chimp genome paper give 5 million indels, totaling ~90 million bp. That's 18 bp per indel, not 300.

It was the Chimpanzee Chromosome 22 paper and it was just a for instance, not meant to be a mean average. However, if the actual LCA was 5 mya instead of 7 mya (which seems to be the consensus) then we are pretty close to where we started. Now it's 18 bp (apparently I don't know what that is because I thought it was base pairs), which is two less then I was basing my earlier estimate on.

quote:
No, I'm trying to tell you that every generation there were ~50 single nucleotide substitutions fixing and 7 indels fixing.

Let's just say that's around 200 base pairs fixed because that sounds like what you are saying. Obviously that would be happening at random in chimpanzee genomes on the same scale and at the same rate. Why did the human lineage have their brain size triple while their primate cousins stayed in relative stasis? I only ask because the LCA was supposedly 5-7 mya and our ancestors did not actually leave Africa until about 1.5 mya. That means that both lineages are contemporary for millions of years, one adapting like wildfire and the other lineage in stasis.

By the way, did you ever notice that none of the fossils found in equtaorial Africa are ape ancestors, only hominids?

quote:
You may be convinced of that, but in reality you've made numerous errors in basic biology and genetics.

I think it's more like fundamental dogma and some kind of a semantical shell game. The issue of adaptive evolution is the lineage leading up to humans must never be challenged, especially if it's based on religious conviction. I make a couple of semantical errors about amino acids, triplet codons and something trivial about the etymology of 'Biology' and I'm guilty of numerous errors.

The genetic basis for the human brain adapting from that of an ape ancestor either does not exist or is completly unknown. That doesn't stop anyone of you from preaching common ancestry like it's an inerrent canon of biology.

I am supposed to take the ubiquitious common anscestry of all living systems back to primordial bacteria and fauna but believing that Genesis 1 through Revelations 22 is history from beginning to end is ignorant. It is logical, reasonable and scientific to accept that randomly occuring mutations somehow managed to produce alterations in highly conserved protein coding, regulatory and funtionally important genes adapting an ape brain to modern humans but it is an argument from incredulity to suggest anything otherwise.

This happens at every major epoh of natural history and don't you dare challenge the assumption that the order and complexity of all living systems were ordered out by exclusivly naturalistic processes. It's ok to believe in God as long as he isn't going to do something inexplicable or supernatural.

I have read the books, webpages, papers and endless posts like the one in this thread for better then two years now. Then I am informed by unanimous consent of scientific professionals I don't have a clue about the basics.

I'm through with it.

Grace and peace,
Mark

Edited by eggasai, : transcript error


This message is a reply to:
 Message 85 by sfs, posted 10-31-2006 2:28 PM sfs has not yet responded

Replies to this message:
 Message 91 by Wounded King, posted 10-31-2006 6:22 PM eggasai has responded
 Message 92 by kuresu, posted 10-31-2006 8:46 PM eggasai has not yet responded
 Message 93 by CACTUSJACKmankin, posted 11-01-2006 9:16 AM eggasai has not yet responded
 Message 97 by RAZD, posted 11-01-2006 9:37 PM eggasai has not yet responded

  
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