Re: Humans, chimps, wheat and frogs

On Dec 4, 12:14 pm, seanpitnos...@xxxxxxxxxxxxxxxxxxxxxxxxxxx wrote:
On 3 Dec, 20:50, hersheyh <hershe...@xxxxxxxxx> wrote:



It is of course entirely possible for two speices to have eaxtly the
same genes, nucleotide for nculeotide, and yet if one of them has a
large inverted section in a critical area, they won't be able to
produce viable offspring.

Not true.  You don't seem to understand the difference between meiosis
and mitosis.

I do. You, however, have a simplistic view of what happens when there
are chromosomal rearrangements like inversions.

Really . . .

For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced.

It is true that *when* there is a crossover within an inverted region,
for the two (out of four) chromatids involved in the crossover that
you do get duplication or deletion of information and, depnding on the
location, acentric and dicentric chromatids.
No chromosomal aberration in meiosis occurs if there is no crossover
within the inverted region.

That's right.  It is only when the inverted region is likely to
sustain a crossover event that there is usually a problem.  This is in
fact commonly a problem for mules.  That is why, although there are
rare reported cases of mule fertility, that mules are considered
sterile.

So for those meioses in which crossovers occur within an inversion,
half of the time, *in theory*, you might get an inviable gamete.

More than have the time, far more, depending on the likelihood of a
crossover event within the inverted region.

Depends on the number of crossovers within the inversion. If there is
only one crossover, then only two of the chromatids are affected.
Hence one half. If there are two or more, then what we get depends
upon whether there are two, three, or four strand events.

For a simple understanding of the consequences, see:

http://www.med.nyu.edu/sackler/genetic/Translocations_and_Invers.htm

 *In
practice* it depends on the species.  In corn, for example, dicentric
chromosomes break, leading to the possibility of an egg getting an
aberrant chromosome (and half of pollen getting aberrations).

Dicentric chromosomes aren't the same thing as chromosomal
inversions.  If one chromosome is dicentric and the other is normal,
of course half of the gametes would likely be aberrant.

When you have a paracentric inversion and a crossover within that
inversion, you generate both an acentric fragment that gets lost and a
dicentric chromosome that either gets trapped or gets broken.
See:
http://www.med.nyu.edu/sackler/genetic/Translocations_and_Invers.htm

With really complex inversion, crossing over is actually suppressed
within the inverted region.

In
Drosophila, OTOH, dicentric chromatids do not break and typically wind
up in the polar bodies rather than the egg.  And produce ineffective
double-headed sperm. So the aberrations do not reach the stage of
being in the gametes, whereas the chromatids not involved in crossing
over do get into functional sperm and egg.

There is still a reduction in normal gamete production.  The offspring
would be normal in such a situation - both viable and fertile.

Yes. And the loss in fertility often would be small because the
capacity to produce sperm and eggs far outstrips the number that get
used or survive. After all, in the evening primrose, which has
multiple translocations producing ring chromosomes at meiosis, half of
the fertilized zygotes die early in development.

This is completely irrelevant to the reason why breeding between some
creatures, like donkeys and horses, produce viable, but not fertile
offspring.

Meioses in which there has been no intra-inversion crossing over
produce perfectly normal eggs and sperm in perfectly normal amounts.

That's right.

The reduction in fertility, then, is a lot less than one might expect
*unless* there are multiple or very large inversions.

Why would one expect a significant reduction in hybrid fertility
unless there are multiple or large inversions?  Who is suggesting
otherwise here?

All you said was:
*******
For example, if a piece of donkey chromosome is inverted relative to
its counterpart in horses, then gene-by-gene pairing cannot occur
without elaborate looping and twisting. The chance of a successful
cell division is very much reduced.
*******

No mention, even, of the requirement that there be crossing over, much
less that there be *multiple* rearrangements.

 Significant
reduction in fertility often requires multiple chromosome
rearrangement, not just one.

Only one is required if it is large or in a place of prominent
crossover events. Of course, multiple inversions would increase the
odds of hybrid infertility.

BTW, there are multiple rearrangement differences between humans and
chimp, but as the mule (and the more pathetic hinny) shows, that does
not prevent viability of the hybrid.  

Exactly . . .

For the reason why humans and
chimps do not produce viable hybrids, you have to look elsewhere.

LOL - Right.  The reason is obviously that there is an informational
disconnect between humans and chimps that is not present between
horses and donkeys.  The genetic information of the chimp is telling
the growing embryo to do one thing while the information of the human
is telling the embryo to do another.  The conflicting orders result in
a non-viable embryo.

But such disconnect does not necessarily require massive changes in
the genome. It can occur because of a single mutational difference.

So, the mule cannot make egg or
sperm cells. Thus, the mule is sterile.  However, a mule can still be
born healthy because such growth of non-meiotic cells occurs via a
different process called mitosis.  Mitosis does not have to match
things up; it only has to make copies. So, inversions and
translocations do not prevent the mule from growing up to be an adult..

Perhaps a little refresher course in genetics is in order?

Yes. You do need to take one.

LOL - I've taken many.  What you need to do is to try to stick on
topic instead of throwing around a bunch of irrelevant red herrings.

http://www.detectingdesign.com/donkeyshorsesmules.html

So your entire assumption (interfertility
equals identity of "genetic information") is just a BS assumption on
yourn part that you can't demonstrate in any way whatsoever.

You just don't understand the genetics involved.

You've still not answered the most basic elementary of questions:  How
do you measure this "distance in sequence space", and how can you
therefore show that humans and chimps are further apart in it than any
other two species are.

I've already told you several times.  You can know that they are
likely further, but by how much is not knowable yet.  

What we know is that there is no sequence difference in any gene or
even any length of DNA sequence between chimps and humans that is
unaccountable for by the known rates of change that can be permitted
by selection for change.

Not true.  There are lots of unique miRNAs and other non-coding
elements between humans and chimps that collectively represent a
sizable percentage of the total genome.  How these non-coding elements
interplay to produce end-structure differences that are potentially
quite significant in both structural and functional uniqueness is not
completely understood.  Therefore, it cannot be said that
significantly complex functional differences do not exist in a
qualitative manner.

Do you know of any *qualitative* phenotypic difference between humans
and chimps? I don't. I see lots of *quantitative* differences. And
a fossil record that shows some of the intermediate quantitative
stages in the transition, say between a chimp and human cephalic index
or degrees of bipedality.

So now you are imagining or positing complex functional differences
that are qualitative in nature without the slightest evidence *at the
phenotypic level that we can actually observe* that there is such a
thing? Sort of like your imagining bacteria that include total
sequence space within their teeny little bodies.

Come on. Give me an example of what you mean by a *qualitative*
phenotypic difference between humans and chimps. And why that
*qualitative* difference requires the instantaneous spontaneous change
in all the miRNAs.

The fact remains that the *quantitative* amount of difference between
humans and chimps is mostly selectively neutral with only a few places
where there is a need to invoke selection. And the fossil record is
not one of qualitative intermediates, but only of quantitative
intermediates. I see no reason to invoke the unlikely idea that for
some un-named and apparently invisible and unobserved qualitative
phenotypic difference that one must have a thousand instantaneous
mutations in a whole bunch of *regulatory* elements. Call me when you
have a candidate. Until then all you have is a hopeful wish without
even the supporting evidence of a potential candidate phenotype.

 In fact, there are almost no genes or
lengths of DNA with more change than would be expected by neutral
drift from a common ancestor in the time available. There is nothing
in the amount of change in DNA sequences between human and chimp that
requires non-natural or exceptionally rapid intervention by an outside
agent, intelligent or otherwise.

You don't have enough information to make this claim.

Sure I do. I said that there is nothing in the *amount* of change in
DNA sequences that requires non-natural or exceptionally rapid
intervention by an outside agent. You are positing that *hidden
within* this *amount* of change that could occur naturally there might
possibly be some unknown qualitative phenotypic difference that
required the simultaneous, but individually small, change in a
thousand (or whatever) miRNAs. This is claimed without your being able
to specify even a possible example of a qualitative phenotypic
difference between humans and chimps. It isn't like one cannot
observe these organisms.

The functional
differences and the underlying genetics upon which these are based are
not adequately understood yet.

Any examples of qualitative differences that do not amount to wishful
thinking?

You know that
they are further because they cannot produce viable much less fertile
offspring.  Try to remember this time.

In the case of human and chimp, the reason for inviability of hybrids
would most likely lie in differences in rates of development of
various organs leading to early lethality due to developmental
discord.  It would not be due to chromosomal rearrangements.

You've just made my point for me.  The lack of hybrid viability is not
due to chromosomal rearrangements, but is most likely do to
incompatible informational differences between the genomes.

Yes.

 Again, my
entire argument is that informational differences, qualitative
informational differences, are what should be used to define species
in a more objective manner.  As it currently stands, species are not
defined by unique qualitative genetic differences, but often
quantitative genetic differences.  That is why the term "species" is
so subjective as to be hardly useful in science at all.

What you mean is that the reality of species and speciation do not fit
your religious ideology.

Sean Pitmanwww.DetectingDesign.com

.

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