Re: Humans, chimps, wheat and frogs



Seanpit wrote:
On 4 Dec, 08:05, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:
seanpitnos...@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 bullshit" 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?

It is fine to have your "reasons". It is just that not everyone in
mainstream science agrees with you on this one. Of course, that's
fine. Obviously, most in mainstream science don't agree with me on
many ideas that I think are perfectly "reasonable".

So, anyway, add me to the list of those who don't think your reasons
are reasonable in this particular case. You can't just discount
insertions or deletions of DNA in one genome relative to another as
obviously being informationally irrelevant when we know that more and
more these very same differences are actually functional - and
possibly uniquely functional on an individual or collective basis.

I don't know what you mean by "informationally irrelevant". Nor do I suggest discounting indels. I just think counting each base of an indel as a separate difference, equivalent in value to a base substitution, is silly. If you're going to count, count mutations.

After all, based just on mutational differences alone, regardless of
the size of the difference, modern humans can be just as distantly
"related" as humans and chimps - yet these modern humans can can still
interbreed to produce viable and fertile offspring.

Even if you put "related" in quotes, that isn't true.

"With the decoding of complete human genome, scientists have now
concluded that we are not as similar genetically as we thought we
were: people share perhaps 99 per cent, rather than 99.9 per cent, of
their genes."

What does this actually mean? As written, it makes no sense.

Indian J Physiol Pharmacol 2008; 52(2) : 103–105
http://www.ijpp.com/vol52_2/103-105.pdf

This discrepancy is likely due to the fact that mutation rates in
human genomes are far greater than previously though - by an order of
magnitude.

So you may believe. But why are you going off on this odd tangent? Is it just that we have come within attraction range of one of your obsessions?

"The mean µ in cells from normal donors was 10.6 x 10^–7
mutations per cell division (range 2.4 to 29.6 x 10^–7)."

http://cancerres.aacrjournals.org/cgi/content/full/65/18/8111

See also: http://www.nature.com/nature/journal/v430/n7000/full/nature02697.html

Clearly then, the argument of clear species delineation based only on
the gross numbers of genetic differences without any regard to the
quality of those differences is a gross oversimplification of the
concept of "relationships" between different living things.

Agreed. That's why nobody uses the gross numbers of genetic differences to delineate species. It's another of your strawmen. Again, I'm not sure what you mean by "relationships", in quotes.

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.

Yeah - and modern humans can have this many individual mutational
differences with the next-door neighbor when it comes to absolute
numbers when one isn't concerned about the quality of the difference
(i.e., size and/or functional features).

What do you mean by "this many"? Are you claiming that next-door neighbors can differ by as many as 40 million mutations? Show me some evidence for that claim, if so.

A difference of 1000bp could be functionally significant, and so could a
single point substitution. So?

That's the really important question. That's what isn't adequately
known at this point. The only thing that is clear is that there is a
clearly difference in viable hybrid production.

What is your point, if any?

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.

It could be more or less functionally important. That's what you're
"method" doesn't consider.

Nor does any method so far devised. What is your point?

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.

The meaning is a potential meaning. We just don't know enough yet.
However, the potential biological meaning cannot be dismissed out of
hand either - like you are trying to do. You simply do not know
enough to adequately say, "The estimate is biologically meaningless."

Yes I do. And so do you. You just like that estimate because it inflates the amount of difference, and you want to emphasize differences. You could achieve the same effect by multiplying by 10, with as much biological meaning. A thousand-base indel is not much more likely to be functionally more important than a one-base indel. Even if you're looking for some measure of functional genetic difference, Britten's measure is no more similar to such a measure than is counting only mutations or homologous base differences.

At best you can say that you just don't know if there or isn't a
significant biological meaning. Beyond this, there does seem to be a
significant biological meaning given the fact that no viable much less
fertile hybrids can be produced. It is also likely that such
differences explain certain key structural and functional differences
as well - like those seen in the brain down to the cellular level.

Here you seem to have abandoned the distance measure entirely and gone off into your own obsession. As I said, functional difference is not strongly correlated with genetic distance, by any of the measures so far proposed. You may imagine some kind of functional genetic distance measure, but there is none, at least yet. No matter how much you want to imagine one.

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.

That's right.

If that's what you mean, why can't you just say it?

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.

It isn't wrong.

Yes it is. Let's review. You said "This 98.5% number is usually based on homologies of protein-coding genes." Remember now?

And, my definition of functional informational
complexity is quite clear - a system of beneficial function that
requires at least a certain size and specificity minimum.

It's operationally useless, and completely unclear. It's unquantifiable, and I bet no two people would come up with the same estimate.

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's what I'm saying.

Then why did you say what you said? Do you even remember what you write from one post to the next?

It depends upon what region or type of DNA
you're dealing with. If you dealing with a region that is especially
important in governing the production of a significant phenotypic
difference, you're going to get a greater genetic difference as well.
This is why doing it your way is essentially meaningless. You way
could be used put certain groups of modern humans under different
species classifications. It is scientifically meaningless as you
apply it.

Sorry, too many ambiguous referents here. You seem incapable of clear writing. I don't know what "my way" is, or how it could be used to split humans into multiple species. (Incidentally, you still seem to be laboring under the delusion that species limits are determined by genetic distance.) I don't know what I'm claimed to be applying or why. Or what a "region" is, or what is expected to show greater genetic difference.

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.

The fact that a particular system requires multiple genetic elements
to produce it is not in question here.

Yes it is. You claim that the human brain must have emerged fully formed at the creation, because there can be no functional intermediates between an ape brain and a modern human brain. That's your whole argument, such as it is.

A flagellar system requires at
minimum dozens of individual "genes" to produce it. This is a fact
regardless of how these individual genes were produced. Now, you
think they were produced by RM/NS. You believe this without any
demonstration of the production of any novel system of function that
requires at least 1000 fsaars. You also have no statistical basis for
this belief of yours. You have nothing but just-so stories. That's
it. That's not science. The very same thing is potentially true when
it comes to systems that are based on the input of multiple miRNAs.

I know flagella are one of your obsessions, but try to stay on track here. You have no evidence for the "irreducible complexity" of the set of miRNAs you're looking at, or of the human brain.

[snip Sean's "baffle with bullshit" 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.

Only by your personal definition of genome "relationships".

It's the standard definition. Relationships are genealogical. Ancestors. Descendants. Your genome is related to mine through descent with modification. On that we agree. Your genome and mine are related to those of chimps in exactly the same way. On that you disagree, but don't claim it's my personal definition rather than the standard scientific definition. And again you haven't helped; I still don't know what a "kind" is.

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?

I don't know about "all", since these sorts of things are often
subjectively determined. However, I would say that many members of
Anatidae family do share the same essential gene pool.

Swan-Goose hybrid:
http://elibrary.unm.edu/sora/Auk/v045n01/p0039-p0040a.pdf

Domestic Duck x Domestic Goose hybrid:
http://en.wikipedia.org/wiki/Bird_hybrid

Talk about begging the question! You ask me to provide evidence of hybridization between species with different qualitative functional features, yet you consider the mere fact of hybridization to be conclusive evidence of a lack of such differences! It's therefore impossible for me to present an example, by definition. Do you understand how your reasoning is hermetically circular?

I agree with you that the judgment is subjective; but of course that makes it operationally useless.

Ducks and geese have huge genetic distances, by the way, much much more than that between humans and chimps by any measure you care to try.

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?

You have to know something about the actual functional systems in both
creatures in question. This is not yet know to an adequate degree for
either humans or chimps. All that is known is that there is very
likely some significant functional differences due to the fact that
viable hybrids are not produced.

Again, begging the question. You asked me to provide an example of hybridization despite functional differences, or lack of hybridization despite no functional differences, but your sole evidence for such differences is lack of hybridization.

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.

Only someone as arrogant as you would interpret this as an admission.

Only someone as clueless as you would require a smiley to understand irony.

You have to know that I think you are way off base in just about
everything you say. You're arguments are strained and confused and I
think many are throw out there just to see if they will fly - like a
bunch of BS.

For the record, I never do that.

But hey, you stick to your guns and you say it like you
see it. I like that about you. I think you're at least genuinely
honest in your beliefs - - for the most part.

And I don't think you are. I think you're a biblical literalist who is merely pretending it's all about the science, nothing more. Perhaps you conceal this from yourself and so can be considered in some sense sincere. But you're lying to somebody.

.



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