springcyclone.bsky.social
PhD in genetics using C. elegans #teamworm | She/Her/Hers | chromatin, condensin, gene regulation, teaching, advocacy
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NIH has been intentionally holding up grants including non-competitive renewals.
This “pause” should be evident in Reporter data over the next week, but I posted about the beginning of it yesterday.
This is now ending because “NIH” has put a process in place to evaluate grants.
2/n
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But this was wild and it wasn’t just asked once
Multiple kids asked this and I need to know where this is coming from bc wtf
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I told them NO (I wanted to say fuck no) and then went into a whole thing about the human genome project being volunteers that was aggregated, and also about ethics in research, the National research act of 1974, how prisoners are vulnerable populations and we apply extra protections to them
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That’s a waste of maple syrup
Use high fructose corn syrup!
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Thank you! 🥺
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By demonstrating that condensin I-DC has an active ATPase that's required for dosage compensation, we hopefully apply these findings to other scenarios where condensins mediate gene regulation
#condensin #generegulation #chromatin #celegans 🪱
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Dosage compensation in worms is a paradigm for chromosome-wide gene regulation by a condensin as C. elegans don't completely shut down one X like mammals. Instead, each X is downregulated to have 1/2 expression by condensin I-DC and together both X's = single male X.
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We also found that loss of this function can prevent condensin I-DC from strongly binding DNA but it is random, leaving 2 populations – strongly DNA bound and weakly DNA bound, contributing to the lack of dosage compensation and maternal effect lethality in offspring
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The in vitro biochemistry demonstrates that DPY-27 can hydrolyze ATP and that the EQ mutation abolishes this function
Our mutant worms demonstrate that losing this ATPase function is equally severe to losing the functional protein (EQ vs indel worms).
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But then I threw a wrench into the whole story by saying "let's do the in vitro biochemistry" 🤡 our lab is a not a biochemistry lab so I had to learn everything from the ground up 🙃
(there were some days of lying on the ground and contemplating existence)
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So Dillon, our tech, made the mutant worm 🪱
We actually ended up with 2 worms, the ATPase dead mutant (EQ) and an insert-deletion (indel) which phenocopied other condensin null mutants. We decided to use the indel as comparison for the ATPase dead mutant
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This question came out of a debate – is condensin I-DC an active condensin OR is it just a scaffold for the rest of the dosage compensation complex?
So we said, let's kill the ATPase and see what happens. Luckily for us, DPY-27 is really similar to other SMC proteins