pjie2.bsky.social
Father, husband, scientist, singer. Prone to getting over-excited about nerdy stuff in public. He/him.
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Add on the fact that in these evolving annelids becoming terrestrial, there's going to be a massive change in the selective environment for sperm AND additional stressors that can cause DNA fragmentation - I'd say that's as good a starting hypothesis as any to explain the pattern seen here.
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Ergo, survivable translocations that create viable heterozygous F1 organisms are more likely to be due to mutations that occur in postmeiotic sperm cells.
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BUT! Egg cells have no extended haploid phase. Sperm do have a haploid phase, sperm chromatin is vulnerable to breakages from oxidative stress and the mechanical processes of condensation, AND any breakages have to be repaired by error prone NHEJ or MMEJ since there is no template for HR.
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But if mutations occur postmeiotically, not only have you already passed all the meiotic checkpoints, but the resulting gamete is guaranteed to be euploid. It starts and finishes with one copy of everything, even if it reshuffles the contents during the process.
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If the mutation occurs as part of meiosis, then the same considerations largely apply depending on the precise timing in relation to checkpoints - still have the issue that meiotic translocations will usually generate aneuploid gametes.
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If the initial mutation occurs premeiotically, it will cause issues with meiotic pairing, so many changes will get immediately filtered out removed by meiotic checkpoints. Even if not removed, missegregation at meiosis means a high proportion of the resulting offspring will be aneuploid / nonviable.
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Any heritable rearrangement must occur in the germline. So then we can look at the barriers in place from the initial mutation through to the generation of an F1 organism heterozygous for the rearrangement.
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We advance a similar argument here to explain why EBRs across rodent phylogenny by and large correlate to 3D chromatin structure in spermatids.
pmc.ncbi.nlm.nih.gov/articles/PMC...
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Thinking about it, desiccation in gametes could create DSBs and structural rearrangements - and if it occurs / repairs in the gamete then the diversity is being generated AFTER the meiotic checkpoints that might eliminate it, and you're also guaranteed that the F1 with the rearrangement is euploid.
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Not that mixed, unless you mean the size of the explosions
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That wouldn't itself generate structural diversity, but it might give strong selective pressure to favour structural rearragements that lock together haploid-selected supergene complexes.
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How does fertilisation differ between land- and water-based #annelids? Having to evolve a new system certainly opens up a window for high levels of haploid competition between gametes.
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That was partly my reasoning :-)
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And Linda Smith
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... & it's not just Oxbridge, Imperial, LSE, UCL etc. Depending how counted, UK has 170 unis, 10 in world top 100, 90/top 1500, & all/top 3-4K: amazing in context of 20-30K unis world-wide. Many countries would beg for such riches (in many senses) & we're almost casually letting them wither away 2/2
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If not, there’s a genetic engineering project for an unlucky postdoc ;-)
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Further thought, aren't we lucky Mendel chose peas rather than roses?
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Can all four of the different subgenomes be diploid in different roses, or just the S1 for canina and the R2 for rubiginosa? Are S2 and R1 ever diploid?
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This is gorgeous and mad and I both love it and am EXTREMELY glad I don't study plant genetics.
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I would read it, but I can't sign in - my institution isn't listed so I can't set up an account. Guess my research isn't professional enough :-(
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Any chance she was paired?
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Oh god what now?
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Living things (which started off alive and then continued to be alive) evolving when put under selective pressure is literally the least surprising outcome in all of biology.
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Sure, and the type of functions they can evolve their organoids towards are interesting in some ways - but in terms of ‘a new state between life and death’? That’s purest bullshit.
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The threshold for ‘normal’ sperm morphology in human males is 4% normal forms.
In other words, up to 96% malformed sperm is ‘normal’
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Not interesting at all (at least not in the way they're advertising). Any living, reproducing thing will develop new functions if you apply enough selective pressure. A cancer cell line evolving to become drug resistant has acquired a new function.
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Yeah, this is purest drivel from a scientific perspective - snow job to attract funding.
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Counterpoint: candiru
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Judge Young is beyond livid — and fuming. He has another hearing that was supposed to begin minutes ago, and he's still going.
"I've never seen a record where racial discrimination is so palpable. I've been on the bench for 40 years. I've never seen government racial discrimination like this."
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So you get to use it to teach about racism then and now. Bonus context!
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I mean, this is the equivalent of saying you can’t use Jingo to discuss the politics of war, or Night Watch to talk about the ethics of policing.
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Yeah, but if anyone tried to say they couldn’t see that Monstrous Regiment had anything to say about gender roles, I’m sure he’d have been equally terse.
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That is pretty much the extent of all the information and theory we have (or ever CAN have) on the subject.
While academics can and will keep arguing AT LENGTH about the details, the only real answer is, “Maybe, I guess?”
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So it’s still very unclear whether there’s an evolved purpose to menopause or whether it’s a side effect of ‘recently’ increased lifespan - which in evolutionary terms means a change over millions of years, not thousands.
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Chimps *do* have a menopause if they live long enough, but living that long seems to be pretty rare in wild chimps.