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Genetic basis for human evolution

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rmwilliamsll

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to get back to the second piece of the OP about HERV's.

i had a virology class in the late 1970's the prof announced one lecture that we were going to skip the chapter on retroviruses because there were no medically significant retroviruses.

that is how new and how important the information on HERV's is.
one- they duplicate the clades we have for physical similiarites which forms the basis for the taxonomic system we use.
two-they duplicate the clades from protein and gene similiarities.

next HERV's like HERV-W destroy the AiG/YECist argument of no new genetic information. despite the vagueness of their definition HERV-W show not only the importation of new dna into the human genome but it's co-option to do a job in the functioning of the placenta.

handling the data properly is important.
 
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KerrMetric

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The Lady Kate said:
Mark Kennedy: "Here's my refutation of an evolutionist article."

Kerrimetric: "Your 'refutation' is based on a stunningly obvious error in calculation which, when corrected, shoots down your entire argument....which has happened before."

Vossler: "hey, cut the guy some slack! He's a fellow Chistian!"

Not quite. I was being a tad pedantic. Mark really never gets around to stating his real problem clearly but I'm sure he means the mutation rate required is greater than he feels is possible. It isn't but that is another debate.

I was pointing out that if Mark is so learned then the basic error he does commit is very telling about his acumen in technical areas. I have seen him commit these basic errors before.

Vossler on the other hand just knee jerks praise at anything and everything pro-Creationist no matter what regardless of the 'technical' content.

The reason I said I was being pedantic is because my comment really doesn't refute his assertion per se - it just points out he makes very basic errors that someone technically versed would not possibly make.
 
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shernren

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Re this:
one- they duplicate the clades we have for physical similiarites which forms the basis for the taxonomic system we use.
two-they duplicate the clades from protein and gene similiarities.


I am lost.

And is a mutation rate of 25 bp/year really very high? It doesn't seem so to me looking at a genome with lengths measurable in Gbp.
 
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rmwilliamsll

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shernren said:
Re this:
one- they duplicate the clades we have for physical similiarites which forms the basis for the taxonomic system we use.
two-they duplicate the clades from protein and gene similiarities.


I am lost.

And is a mutation rate of 25 bp/year really very high? It doesn't seem so to me looking at a genome with lengths measurable in Gbp.


there is a nicely drawn clade/Phylogenetic Tree at: http://www.sciencedaily.com/releases/2005/03/050328174826.htm
 
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gluadys

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shernren said:
Re this:
one- they duplicate the clades we have for physical similiarites which forms the basis for the taxonomic system we use.
two-they duplicate the clades from protein and gene similiarities.


I am lost.

The classification system devised by Linneaus was based on physical similarities. It is a nested hierarchy.

With the discovery of DNA sequences, scientists have been able to relate species on the basis of gene and protein similarities. This classification also results in a nested hierarchy. But even more important, this second nested hierarchy, which has not taken physical similarities into account at all, turns out to match the one that is based on physical similarities.

One can also use features like ERVS to generate a phylogeny. And lo and behold, they too lead, not only to a nested hierarchy. They duplicate the clades based on physical, genetic and protein phylogenies.

And is a mutation rate of 25 bp/year really very high? It doesn't seem so to me looking at a genome with lengths measurable in Gbp.

When you consider that you can get this amount of change from a single mutation, no. Although most mutations would involve smaller numbers of bp down to point mutations which only affect one bp each.

It is not really the number of mutations that is pertinent though, but the number that become fixed in the species. However, here again, I think Mark is using the number of base pairs as a proxy for the number of mutations. But since the number of bp per mutation can range from one to over a hundred that is not a good proxy.
 
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OldWiseGuy

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(Many) animals and man were created by God to be a walking, talking, lying, stealing, killing, perverse, destructive, hateful, living demonstration of sin. Why shouldn't we be genetically related?
 
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muaxiong

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rrwilliams said:
I don't mean this as a personal put down, for it is not, it is an expression of concern that you are trying to enter into a technical discussion with not just inadequate background but very wrong ideas which make your writings wrong from the beginning.
So what are your credentials?
 
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rmwilliamsll

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muaxiong said:
So what are your credentials?

read carefully what i wrote. it is not a question of credentials, it is a question of understanding what is being read. the posting indicates a lack of basic understanding of what the papers say.

btw.
i have about 300 units of semester credit in undergrad and grad biology, chemistry, philosophy, a BS from UCSD in biology, the rest of the units from work on a second BA at the UofAZ. just to answer your question. i can read technical papers in my fields of study. but am open to criticism and correction, as is anyone cognizate of the difficulty of technical understanding. plus i post my reading lists to the net and review what i have finished on amazon. i keep a master list of essays i've written on the subject and interact with people on the issues.

are you this transparent and educated in the fields? do you spend upwards of 40 hours per week reading on the topic? if you desire to play the game of "whose is bigger?" what are your credentials? if you have a PhD in molecular biology does that give your postings here greater weight? yes, at least with me, but they must have the internal evidence of understanding the things that they handle or someone will challenge you on the errors. as they will do in any professional paper or speech you would give. education is not a get out of jail free card in warding off criticism, correctness and truthfulness are.

but again, it is not a question of credentials but of basic understanding evidenced by a lack of ability to engage properly with the data. the specifics which has in this case been pointed out by several people.

discuss the issues, not the personalities behind the postings. both the math in the first half of the OP and the HERV's statements in the later half were "not just wrong".
 
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Athene

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Right ok, I see where Mark is mistaken, Mark. 1 Mb is equivalent to 4 million nucleotides exactly.

What you are doing is adding 90Mb of data too 35 million nucleotides and claiming this equals 125 million nucleotides, which it doesn't, it would be something like 360 million nucleotides.

And you're also assuming that all the indel events which make up the 90Mb difference between chimps and humans is down to single insertion or deletion events, this is not so, there are only 5 million actual events but many of the events involve blocks of nucleotides greater then 15 kb.
 
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Pats

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KerrMetric said:
I'm sure he means the mutation rate required is greater than he feels is possible. It isn't but that is another debate.

It seems to me that you've finally spoken to the actually issue raised in the OP and then differed answering it by claiming it's another debate.

What's this debate?

It seems it was taken way off topic and hasn't returned. I'd enjoy hearing answers to the mutation rate required for common ancestory to be viable.
 
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Athene

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Mark is mistaken in his calculations, I did address this in a previous post but reading back I hadn't made it particularly clear.

Marks mistake was too add 90Mb of data to 35 million nucleotides, giving him a number of 125 nucleotides, but you can't do that, 90Mb is a measure of the information which is related to the number of nucleotides. 90Mb of information corresponds to something like 360 million nucleotides. But you still can't add the 360 million to the 35 million because . . ..

This doesn't mean there have been 360 million individual mutations, we're not talking about SNPs here, we're talking about indels, insertion and deletion events which involve blocks of nucleotides which could be several thousand bases in length. In an insertion a block of DNA is added to the genome, a deletion is when a block of DNA is removed, the number of nucleotides added or deleted is not particularly important, what is important is the number of such events, which the authors of the article have estimated to be 5 million.

So if I wanted to calculate the rate Marks way that would be (35+5)/5 = 8

8 mutations a year - divided between 2 populations of several thousand each . . .. . not a great deal is it?

(though that method of determining rate seems too simplistic to me, does anyone know how mutation rate over time is calculated?)
 
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gluadys

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Athene said:
So if I wanted to calculate the rate Marks way that would be (35+5)/5 = 8

8 mutations a year - divided between 2 populations of several thousand each . . .. . not a great deal is it?

(though that method of determining rate seems too simplistic to me, does anyone know how mutation rate over time is calculated?)

I don’t know about measuring mutation rate, but reputable sources say that in mammals it is about 120 per replication. That is many times more than Mark thinks is impossible, even when you limit it to germ-line mutations.

But mutation rate per se is not the relevant figure. The relevant figure is fixation rate. How many of those mutations become fixed in a population as the norm for the species? Mutations happen in individual cells. Fixation means a mutation is spread from the first individual in which it occurs to over 95% of the population. Fixation is obviously much more rare than mutation. And the base-line for calculating fixation rate is much more controversial. Nevertheless, there have been attempts at calculating not just mutation rates, but rates of evolution. There is even a unit of evolution called, appropriately, a “darwin” which refers to how much divergence occurs within a set time frame. (100,000 years, I think, but it could be more.)
 
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shernren

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Ok. I think Mark's initial comments aren't really very valid, sorry to say :p but let's hear some comments about the article he cited ... I'm quite curious to know what the article means when it says something about the endogenous retroviruses being extinct, I don't quite get that. And of course, we can push some really scientific questions on this:

1. What does evolution predict?
2. What do we observe?
3. How do they match up?

based on the report. Layman's English encouraged but not compulsory. :p
 
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rmwilliamsll

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shernren said:
Ok. I think Mark's initial comments aren't really very valid, sorry to say :p but let's hear some comments about the article he cited ... I'm quite curious to know what the article means when it says something about the endogenous retroviruses being extinct, I don't quite get that. And of course, we can push some really scientific questions on this:

1. What does evolution predict?
2. What do we observe?
3. How do they match up?

based on the report. Layman's English encouraged but not compulsory. :p


the article is at:
http://www.nature.com/nature/journa...l;jsessionid=6D7F4581FB469D25680C6C69275794D9

the quote you reference is
Endogenous retroviruses. Endogenous retroviruses (ERVs) have become all but extinct in the human lineage, with only a single retrovirus (human endogenous retrovirus K (HERV-K)) still active24. HERV-K was found to be active in both lineages, with at least 73 human-specific insertions (7 full length and 66 solo long terminal repeats (LTRs)) and at least 45 chimpanzee-specific insertions (1 full length and 44 solo LTRs). A few other ERV classes persisted in the human genome beyond the human−chimpanzee split, leaving approx9 human-specific insertions (all solo LTRs, including five HERV9 elements) before dying out.

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (approx5−8) invasions, because the sequence differences among reconstructed subfamilies are too great (approx8%) to have arisen by mutation since divergence from human. It is closely related to a baboon endogenous retrovirus (BaEV, 88% ORF2 product identity) and a feline endogenous virus (ECE-1, 86% ORF2 product identity). The larger family (PtERV1) is more homogeneous and has over 200 copies. Whereas older ERVs, like HERV-K, are primarily represented by solo LTRs resulting from LTR−LTR recombination, more than half of the PtERV1 copies are still full length, probably reflecting the young age of the elements. PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species68.

HERV-K is apparently related to the mouse mammillary tumor virus=MMTV. from sequence comparision between them.

Only four RV are currently know to infect humans:
* HTLV1 - T-cell leukaemias/lymphomas
Tropical spastic paraparesis
* HTLV2 - No known pathology
* HIV 1 & 2 - AIDS
from: http://web.uct.ac.za/depts/mmi/jmoodie/hiv2.html

thus the reason for the "extinct" phrase.

the prediction is basically building clades based on what creatures have which RV's in their genome and how many mutations have occurred within the RV insertations.

there was a beautifully done clade link posted that i am freely referring to at:
http://www.sciencedaily.com/releases/2005/03/050328174826.htm
i found a nice background article on clades at:
http://personal.uncc.edu/jmarks/pubs/marks evanth05.pdf

it may take some time and effort for most people to get through the article, but it is worth a read.
 
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Athene

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I goofed, Mb stands for megabases, MB stands for Megabytes, the article refers to Mb. But Megabytes are a valid way of measuring the information contained within nucleotides, just not what the authors of the article were using.

But Mark still miscalculatd because it's not the number of nucleotides in the indel that is important but the number of indels themselves.
 
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