Re: Blog: The Scars of Evolution.
- From: hersheyh <hersheyhv@xxxxxxxxx>
- Date: Sat, 22 Mar 2008 10:54:43 -0700 (PDT)
On Mar 22, 2:25 am, Treus <treusd...@xxxxxxxxx> wrote:
hersheyh wrote:
On Mar 21, 7:35 pm, Treus <treusd...@xxxxxxxxx> wrote:
hersheyh wrote:
On Mar 21, 12:01 pm, Treus <treusd...@xxxxxxxxx> wrote:
The situations are not equivalent. Inertial orbits follow
deterministically from a few variables according to _know principles_.
You seem to be under the delusion that, because I am proposing a
completely random process, that I am unable to make predictions wrt
the results.
No, the defect is not its randomness. I am looking at where the basis
for getting your inputs to your outputs should be, and there's nothing
there. You're basically saying macro is just another form of micro
extended over time and thus no additional causal processes are
necessary.
What I am saying is that *all* the genomic sequence difference between
the human genome and the chimp genome represent *ordinary* mutational
differences (point mutations, indels, and rearrangements like those
that can be observed occurring in any organism with a DNA genome) and
that *all* the sequence difference between the human genome and the
chimp genome can be accomplished in the time available by the slowest
possible mechanism, namely neutral fixation of selectively neutral
mutations. *When* selection is involved, the rate of change is much
faster, but the type of mutations are still nothing but *ordinary*
mutational differences. Do you have even a *single* example of some
genome sequence difference between humans and chimps that requires
anything but an *ordinary* mutational change (or several of them)? I
presume that you are under the delusion that "macro" evolution
involves some special magical type of mutation that differs from the
types of mutation seen in "micro" evolution. But until you can point
out some (even one) specific examples to the contrary, I will continue
to claim that *all* the genomic sequence differences between humans
and chimps are due to "ordinary" mutational events. What about the
word *all* don't you understand?
Besides the question is about the *sufficiency* of mechanisms to
account for the difference between humans and chimps. I have already
stated the reasons for thinking that the actual rate of change
required to produce the observed difference will be slightly *less*
than the rate of change that would be due to chance alone. I even
ascribed a causal mechanism to explain the slower *actual* or
*observed* rate of change rather than the *rate* one would expect if
chance were the only mechanism at work. Hint: selection preserving
functionally relevant sequence. The amount of selection involved in
producing *change* in sequence is so insignificant, relative to the
amount of change due to chance alone, that it is basically invisible.
What remains unclear is exactly why you think this, because
you keep referring to the genome as if it can be modified in isolation
without considering the viability of the corresponding organism at
every generation.
No. I am not ignoring the viability of the organism. I said I was
*assuming*, for the sake of determining whether the slowest possible
rate of change was *sufficient* to account for the *observed* amount
of genome sequence difference between two species, that the entire
genome of the two species was selectively neutral (instead of
93-95%). I did that because it allowed me to predict, based on simple
probablistic assumptions, the amount of change that could be produced
by the *slowest* possible mechanism and *test* whether that *slowest*
mechanism was *sufficient* to account for the observed amount of
change.
<snip>
You're claiming two species can be connected through neutral mutations
alone,
No, I am not. I am saying that the slowest known mechanism of change
is *sufficient* to account for the amount of difference between the
two species we are examining. In fact, the evidence is that most of
the sequence in both human and chimp genomes are, in fact, to a large
extent, sequence independent. So most of the differences we observe
are, in fact, due to neutral fixation. The number of sequence
differences that have been due to selective pressures in one or the
other lineage is quite tiny, but those few differences that have been
subjected to such selection for change are crucial to the phenotypic
differences we observe.
and that this would eliminate the nonviability problem but also
slow things down due to the absence of natural selection.
I am assuming, for the sake of testing the *sufficiency* of the
slowest possible method to produce the observed amount of change, that
the entire difference was due to that slowest possible mechanism. I
am quite aware that there is conservative selection for the retention
of function, *which does not produce any differences* and thus is
irrelevant to the question of whether or not there is a mechanism that
is *sufficient* to produce the observed amount of *differences.* I
am also aware that there are a quite surprisingly (at least to you)
number of *differences* that are due to selection for those
*differences*. By assuming that those differences that are due
selection, which fixes change in sequences orders of magnitude more
rapidly than neutral fixation, I am biasing the results against me.
*If* most of the total amount of *differences* between the human and
chimp genome (we are not interested in the similarities) required
positive selection, then the slower mechanism of neutral fixation
would be *insufficient*.
If I've got that right, how many lineal descendants would an organism
need to have before the first member of a new species arrived?
This makes no sense wrt the questions you asked about the
*sufficiency* of known mechanisms and how to test for it. I fully
recognize that humans and chimps are different species *because* of at
least some of the sequence *differences* in their genomes. My test of
*sufficiency* of the slowest known mechanism to account for *all* of
the differences doesn't require me to distinguish or identify those
differences that are selectively important and those that are not. I
do assume that *all* the genome sequence differences can be attributed
to known types of mutation and that mutations that produce selectively
neutral differences and mutations that produce selectively beneficial
or detrimental differences are both ordinary mutations (point
mutations, indels, rearrangements).
Just by
way of illustration. Whatever details you wish to supply an example of
the process will be fine.
.
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