Re: Humans, chimps, wheat and frogs

seanpitnospam@xxxxxxxxxxxxxxxxxxxxxxxxxxx wrote:
On 2 Dec, 19:00, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:
Seanpit wrote:
On 2 Dec, 15:58, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:
Um, humans and chimps are 98.5% identical in their DNA.
Depends on what part of the genome you're looking at. This 98.5%
number is usually based on homologies of protein-coding genes.
Wrong. It's based on the overall percent identity of all sequences with
homologs present in both species. Since protein-coding (and other
conserved) sequences are a tiny minority of the genome, in effect it's
an assay of junk DNA. Protein-coding sequences are on average 99.5%
identical between species.
Most estimates of sequence divergence have focused exclusively on base
substitutions in DNA—that is, one base (or one DNA ‘letter’—A, T, C or
G) being replaced with another. More recent calculations also include
insertions and deletions, or indels, in addition to base
substitutions.
No, those aren't more recent calculations. They're just different. None
of the numbers you have quoted have anything to do with counting indels.
What follows here is more of your "baffling with bull***" tactic. When
you're wrong, you just cite irrelevant studies.

They're published in mainstream literature. I guess you get to decide
what is and is not relevant in science?

We all do. I have stated my reasons. What's wrong with them?

The author of one such study, Roy J. Britten, argues:
"It appears appropriate to me to consider the full length of the
gaps in estimating the interspecies divergence. These stretches of DNA
are actually absent from one and present in the other genome. In the
past, indels have often simply been counted regardless of length and
added to the base substitution count, because that is convenient for
phylogenetics."
Yes, and I think Britten's idea is silly. What biological reason is
there to count the lengths of gaps, when each gap is generally a single
mutation? A 1-base gap is 1 mutation; a thousand-base gap is 1 mutation.

A difference of 1000 bp could be functionally significant - regardless
of how it was produced. That is why Britten's method makes much more
sense than only counting non-gap regions of DNA.

What makes the most sense is counting mutations. Humans and chimps differ by 40 million mutations. 35 million of those are point substitutions. 5 million are indels. There are a negligible few more that don't fall into either category, such as chromosomal fusions, inversions, and perhaps a few more categories I'm not thinking of.

A difference of 1000bp could be functionally significant, and so could a single point substitution. So? I'm not saying you should count only non-gap regions. I'm saying you should count one mutation as one mutation. A 10-base indel is not any more or less a single mutation than a 1000-base indel.

Britten, R.J., Divergence between samples of chimpanzee and human DNA
sequences is 5%, counting indels, Proc. Nat. Acad. Sci. USA 99(21):
13633–13635, 2002.
His findings lend support to the idea that much of the failure of DNA
to hybridize between chimps and humans is the result of missing DNA
due to indel events.
What failure to hybridize are you talking about here? Perhaps you mean
that most sequences that don't hybridize are those that are not shared.
That makes sense, as the other reason for having a non-hybridized
fraction in a DNA-DNA hybridization experiment is high sequence
divergence, which isn't going to happen between humans and chimps.

Exactly . . .

So?

Britten then became involved in a follow-up paper in which these
initial results were confirmed; in fact, it was found that "the 5%
human-chimp difference already published is likely to be an
underestimate, possibly by more than a factor of 2." - - in other
words by more than 10%.
Again, the estimate is biologically meaningless.

How do you know? . . .

Explain its biological meaning.

Britten, R.J., Rowen, L., Williams, J. and Cameron, R.A., Majority of
divergence between closely related DNA samples is due to indels, Proc.
Nat. Acad. Sci. USA 100(8):4661–4665, 2003.
Then, Anzai et al. published a study where nearly one-half of the MHC
region was sequenced - within chimps. The sequence results in
comparison the the human region actually dropped the DNA similarity
estimate down to 86.7%. Anzai concluded that the 86.7% estimate "may
be a better representation of whole-genome sequence similarity between
the human and the chimpanzee" than previous estimates of 98.6% since
"the major difference between the human and chimpanzee sequences is
overwhelmingly attributable to indels".
Once again, biologically meaningless.

Based only on your say so . . .

I have given my reasons. Feel free to argue with them.

Anzai, T., Shiina, T., Kimura, N., Yanagiya, K., Kohara, S.,
Shigenari, A., Yamagata, T., Kulski, J.K., Naruse, T.K., Fujimori, Y.,
Fukuzumi, Y., Yamazaki, M., Tashiro, H., Iawmoto, C., Umehara, Y.,
Imanishi, T., Meyer, A., Ikeo, K., Gojobori, T., Bahram, S. and Inoko,
H., Comparative sequencing of human and chimpanzee MHC class I regions
unveils insertions/deletions as the major path to genomic divergence,
Proc. Nat. Acad. Sci. USA 100(13):7708–7713, 2003.
Of course, other studies, have resulted in estimates of similarity
higher than 98.6%. For instance, Wildman et al.compared ~90 kilobases
of human DNA to chimps and found a similarity of 98.86%, even when
counting indels.
Wildman, D.E., Uddin, M., Liu, G., Grossman, L.I. and Goodman, M.,
Implications of natural selection in shaping 99.4% nonsynonymous DNA
identity between humans and chimpanzees: enlarging genus Homo, Proc.
Nat. Acad. Sci. USA 100(12):7181–7188, 2003.
This seems to be in direct opposition to the data presented by Britten
and Anzai et al. However, Wildman’s team examined only coding DNA from
a number of genes. Britten and Anzai both considered non-coding DNA in
their studies and therefore consider a greater range of DNA types in
their conclusion of an 86.7 similarity.
Blah, blah. More irrelevant nonsense, except that you provide a quote
for my statement that protein-coding regions average 99.5% identity.

Just bricks and mortar - not the main informational source within DNA.

I agree that most of the significant differences between humans and chimps are probably in non-coding DNA, if that's what you mean. I don't know your definition of information, so can't be sure what you meant to say. I just point out that your initial assertion about the nature of that 98.5% similarity is wrong, based on what you yourself have quoted.

See also:
http://www.answersingenesis.org/tj/v18/i2/similarity.asp
However, non-coding functional DNA elements, like miRNA producing
regions of the genome, can be much more different. For example,
miRNAs from the brains of humans and chimps show an overlap of only
83%.
What exactly does this mean? Are you talking about the genome or about
expression patterns?
Both . . .
Not good. You need to untangle them if you want to know what's happening.

Not needed in this case . . .

Why?

"miRNAs recently have been implicated in synaptic development and
in memory formation. As the species specific miRNAs described here are
expressed in the brain, which is the most complex tissue in the human
body, with an estimated 10,000 different cell types, these miRNAs
could have a role in establishing or maintaining cellular diversity
and could thereby contribute to the differences in human and
chimpanzee brain ... function."
http://www.niob.knaw.nl/researchpages/cuppen/publications/berezikov_N...
Ah, it is indeed expression pattern, though they did search the genomes
for recovered sequences. So 83% of candidate miRNAs recovered in this
particular expression study were found in both genomes. Note that many
of these miRNAs are parts of families that have been duplicated, with
divergence, either in human or chimp, so there is a known mechanism
responsible for at least some of the difference. I note also that the
percentage of miRNAs in common between species pairs follows exactly the
pattern expected from phylogeny.
All bets are off when NS is involved as a preserving force over
time. Here we have 17% miRNAs that are not homologous between species
- and that is just one type of non-coding potentially functional DNA
type. This isn't just an expression pattern. This represents unique
genomic differences that are likely functionally important.
Again, it's 17% of the candidate miRNAs that were recovered in a
particular expression study that are not *orthologous* to one in the
other species.

And what reason is there to think that this sampling is not
representative of all miRNAs? - and the underlying DNA sequences upon
which they are based?

What reason is there to think it is? I suspect the brain tissue was chosen for this study based on the assumption that it's not representative, but is a tissue of special importance in human evolution.

That is closer than most of the other species which creationists
assume "microevolved".
It isn't as clear cut as you make it out to be. The functional
differences between humans and apes are not clearly understood on a
genetic level yet.
Well enough that it seems unlikely there could be any huge neutral gaps
hiding in the genetic differences.
You can't say that unless you actually know something about the end-
product functional differences - differences that may be and are
likely the result of many miRNAs and other non-coding elements using
similar gene-product building blocks to build functionally novel
systems. This is in fact suggested to be the reason for structural
and functional differences between the brains of humans and chimps.
And it may be part of the reason. But miRNAs are short and can easily
evolve. We also have no data suggesting that any of this requires
crossing of any large, neutral gap, and every reason to believe that
individual mutations could be selectively advantageous.

It isn't the miRNA's one at a time that is important here. It is the
end-product system that is important here. If the end-product system
requires multiple miRNAs to produce its unique structural features, at
minimum, the problem isn't going to be solved by explaining how to get
one miRNA at a time since a minimum of many are required before the
minimum structural requirements of the system in question can be
realized.

We have no reason to believe that multiple miRNAs must have been inserted simultaneously, or that they couldn't have evolved one at a time. You have no evidence for your claim that a "minimum of many" is necessary. And in fact if this is about brain size, the fossil record shows a gradual increase over millions of years.

[snip Sean's "baffle with bull***" phase]
What? You think the fact that humans and apes do not produce viable
much less fertile offspring is irrelevant?
Yes. Some closely related species can't produce viable offspring. Some
distantly related species can. There is no particular correlation
between closeness of relationship and hybridization.

Ah, care to provide some actual examples?

The problem with this is that I don't know what you are willing to consider related, since I have no idea what a "kind" is supposed to be. But this is a commonplace fact of science.

I say that there is a very good correlation between qualitative
functional aspects of a gene pool and hybridization. Allelic
variations with the same qualitative function aren't in question
here. Many quantitative differences can exist between gene pools -
just as long as the qualitative functional features and options are
the same.

That's fine for you, because the undefined nature of "qualitative functional features and options", being known only to you, makes it possible for you to ignore any examples I might bring out.

But let's try. Does the entire family Anatidae share all the same qualitative functions?

How is the presentation of
examples of interbreeding species that produce at least viable and
even occasionally fertile offspring at all germane when it comes to
the argument that humans and chimps are even more closely related?
It isn't. Nor is the inability of chimps and humans to hybridize.

Think again. One of the very foundations of the concept of
"speciation" involves the ability to successful mate and interbreed.

That was a bizarre non sequitur, and I have no idea how to respond.

This means producing both viable and fertile offspring. If at least
the viability part of this equation is intact in one pairing, but not
another, which pairing most likely represents a more functionally
"close" or "similar" pairing?

I have no idea, since none of your terms are defined. How do we determine functional similarity?

even though they cannot produce viable much less fertile offspring?
Who's BSing here?
You are, as I've already mentioned several times.

LOL - right ; )

Thanks for admitting that, at least.

.

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