Re: Science has a news article up about "living fossils"

On 3/18/24 5:48 AM, jillery wrote:

On Sun, 17 Mar 2024 07:46:53 -0700, John Harshman
<john.harshman@gmail.com> wrote:
 

On 3/15/24 12:45 AM, jillery wrote:

On Wed, 13 Mar 2024 06:28:17 -0700, John Harshman
<john.harshman@gmail.com> wrote:
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On 3/12/24 10:59 PM, jillery wrote:

On Tue, 12 Mar 2024 09:04:22 -0700, erik simpson
<eastside.erik@gmail.com> wrote:
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On 3/12/24 6:44 AM, John Harshman wrote:

On 3/12/24 3:50 AM, Ernest Major wrote:

On 11/03/2024 23:28, John Harshman wrote:

On 3/11/24 4:17 PM, RonO wrote:

https://www.science.org/content/article/these-gars-are-ultimate-living-fossils
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Open access article:
https://academic.oup.com/evolut/advance-article/doi/10.1093/evolut/qpae028/7615529?login=false
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These researchers looked at Gar, but it also applies to sturgeons.
These two bony fish lineages seem to have a very slow rate of
molecular evolution.  The changes in their DNA accumulate so slowly
that two lineages separated for over 100 million years can still
form fertile hybrids.  3 million years is pushing it for species
like lions and tigers that can still form hybrids, but the hybrids
are sterile. Bonobos and chimps are around 3 million years divergent
and can still form fertile hybrids, but the claim is that these fish
evolve orders of magnitude more slowly than mammals.
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The Science news article claims that mammals accumulate 0.02
mutations per site per million years, while these fish averaged only
0.00009 mutations per million years.  For the 1100 coding exons that
they looked at for this study these fish evolve much more slowly
than mammals.
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The news article notes that other "living fossils" such as
coelacanths (0.0005) evolve faster, but slower than amphibians
(0.007).  It sounds like terrestrial animals evolve faster than fish.

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If it's repair mechanisms they hypothesize as the cause of slow
evolution, they really should be looking at junk sequences rather
than just 4-fold degenerate sites. I suggest introns. And if the
introns aren't alignable, well, that kills the theory right there.
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Tree species thought to be separated by tens of millions of years are
known to hybridise. For example Platanus orientalis and Platanus
occidentalis, and also with Tilia, Quercus and Aesculus. In the case
of Tilia I suspect that multiple rounds of introgression has served to
limit the amount of divergence between species. However Tilia does
appear as a short branch in cladograms, supporting the hypothesis that
forest trees have a lower rate of evolution.
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Then again, ducks that are thought to be separated by tens of millions
of years are also known to hybridize, and their rate of evolution isn't
particularly slow.
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All sorts of seemingly long-separated species (both plant and animal)
are observed.  What determines whether the hybrid offspring are fertile,
infertile or sterile?  I found an article on Big Think
https://bigthink.com/the-past/soviet-human-ape-super-warriors-humanzee-ivanov/
describing an unsuccessful attempt to produce a "humanzee".  Fortunately
it didn't work.  The chromosome count is different in humans and
chimpanzee, but does this imply that it's essentially impossible?

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My understanding is, the limiting factor is the compatibility of mtDNA
with nuclear DNA.  As species evolve, mtDNA mutates faster than
nuclear DNA, but they still need to maintain compatibility with each
other.  Organisms where the two are poorly compatible fail to thive or
even to survive.  Over time, isolated populations can evolve mtDNA
that are no longer compatible with nuclear DNA from other populations.
ISTM infertility between isolated populations would be a natural
though not necessarily inevitable consequence of having two separate
DNA pools.
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*********************************
Zhang C, Montooth KL, Calvi BR. Incompatibility between mitochondrial
and nuclear genomes during oogenesis results in ovarian failure and
embryonic lethality. Development. 2017 Jul 1;144(13):2490-2503. doi:
10.1242/dev.151951. Epub 2017 Jun 2. PMID: 28576772; PMCID:
PMC5536873.
**********************************

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That's one of several possible reasons for incompatibility. Some others
have already been mentioned.

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My understanding is there are likely several causes for genetic
incompatibilities.  My impression is chromosome count is among the
least of them.  As long as the important genes line up during meiosis,
it doesn't really matter if the chromosomes are in multiple pieces.
That's why for example the chromosome 2 fusion wasn't as big a problem
for our ancestors as some claim.
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OTOH mtDNA/nuclear DNA incompatibility is an insurmountable problem.
Since the original endosymbiosis billions of years ago, mitochondria
have transferred much of their DNA into the nucleus, in order to speed
their duplication, while keeping for themselves most crucial genes,
for example to regulate ATP synthesis.

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That makes it sound like a purposeful or adaptive process, but maybe
it's just random. In fact mitochondria in most taxa have lost most of
their crucial genes, and I don't see much difference between the ones
they've lost and the ones they've kept. How is cytochrome c different
from cytochrome b, for example?

  The process of reducing mtDNA wasn't purposeful, in the sense of
having foresight.  It was adaptive aka evolutionary, in the sense that
mitochondria which lost genes necessary to regulate ATP synthesis
would significantly compromise the metabolism of the host organism to
which they were a part, and so would be less likely to increase in the
organisms' population.  OTOH mitochondria which kept genes that were
duplicated in nuclear DNA would duplicate themselves more slowly, and
so their host organisms would be less adaptive.
 I'm not familiar enough with mitochondrial respiration to have an
informed opinion as to which genes qualify as "crucial".  My
understanding is cyt c is involved in the electron transport chain
while cyt b and other cytochromes are not.

I'm afraid your understanding is wrong. Cyt b is part of the electron transport chain. While it's true that most of the genes retained by animal mitochondria are crucial parts of ATP production, so are many of the genes lost from the mitochondrial genome after transfer to the nuclear genome. Many of the proteins involved have to be imported into the mitochondrion, which doesn't seem at all optimal. This seems more like constructive neutral evolution than adaptive evolution. Now of course loss of a crucial gene can only be neutral if it's already been transferred to the nucleus, but that sort of transfer is quite common. The usual fate of such transfers ("numts") is to decay over time, but during the short period when they're functional, the mitochondrial gene could potentially be lost.
I would also note that the mitochondria of some non-animal taxa have much larger genomes, retaining many more genes.

Having two separate pools of DNA with different mutation rates
necessarily means that from time to time some gamete fusions will
combine two incompatible pools.  Breeding long-isolated populations
makes that even more likely.  And once two populations are
biologically isolated, for any reason, they necessarily evolve
independently of each other.

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Would that not be true for any pair of chromosomes whose products must
interact, i.e. more or less any pair of chromosomes? I see no reason to
elevate that particular reason for genetic isolation over several others.

 mtDNA is inherited almost exclusively matrilineally, while nuclear DNA
is inherited from both parents.  Also nuclear genes are diploid, while
mtDNA are monoploid.  My understanding is for these reasons,
maladaptive mtDNA mutations are more likely to be fatal than
maladaptive nuclear DNA mutations.

Not sure why matrilineal inheritance is relevant. But diploidy is. Still, some sex chromosomes (Y, W) are also uniparentally inherited, so should cause similar problems. That might in fact be one mechanism of Haldane's rule.
Anyway, diploidy should only partially buffer the system against the effects of incompatibility. There's also room for more imcompatible genes on a nuclear chromosome, thus potentially more pronounced additive effects.