amoyellab.bsky.social
Stem cell biology and all things fly testis
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Congratulations Courtney! Well deserved!
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👋
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Certainly won't miss it! Great science, great location, and the food...
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Ideally, we'd like authors to cite a recent FlyBase publication. There's a blue box with the text "Citing FlyBase' on our homepage that takes you a page detailing how to cite us wiki.flybase.org/wiki/FlyBase...
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So pleased to see this out in print! Congrats especially to Ruoxu Wang, who worked so hard for this! And thanks to @plosbiology.org editors for being responsive and willing to discuss and change their minds.
Link to the paper here: doi.org/10.1371/jour...
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Adding translational control on top of transcriptional control means that cells can respond rapidly to changes in their environment - a need to differentiate, or a space becoming available in the niche - without being "confused" about their identity, as they only translate the "right" set of genes.
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We speculate this is a way to allow cells to maintain flexibility in fate - in classical developmental biology, we call this "specification" where a cell acquires a fate but doesn't commit to it. In stem cells, this means that a cell can differentiate, but retains the ability to self-renew.
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All solved!
BUT, you might ask, why on earth would we have this complicated regulation of translation, when we have perfectly good regulation of cell fate by transcription downstream of niche signals?
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Finally, we show that this pathway controlling translation is key to self-renewal of stem cells, and can even restore stem cell self-renewal when niche signals are lost.
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In other words, eIF3d phosphorylation helps translation initiation through eIF4F, and indeed, in human cells, it modulates the strength of interaction between the two complexes (as shown by Nick Roiuk @mykolaroiuk.bsky.social and Aurelio Teleman @telemanlab.bsky.social )
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This led us to a new hypothesis as to how eIF3d works: whereas previous work showed it is responsible for binding the cap when eIF4F is absent, in our situation, eIF3d phosphorylation and eIF4F act together to maintain stem cell fate.
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We focused on one of the regulators we identify in the screen: eIF3d. Previous work by Amy Lee and colleagues showed that eIF3d is regulated by phosphorylation, by a kinase called CK2. Knockdown of CK2 also leads to loss of stem cells, similar to loss of eIF3d and eIF4F.
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How do niche signals control translation? We screened translation initiation factors by RNAi and found that different factors are required for self-renewal than for differentiation. This means that there is a mechanism to control how translation initiation happens.
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This means that post-transcriptional regulation is important. In fact, we find that translation rates change during differentiation, and that this depends on the niche signal, Upd.
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Stem cells rely on signals from their niche to self-renew. These signals are known to regulate transcription of genes required for self-renewal. But we find that transcripts encoding proteins expressed in differentiating cells are also present in stem cells, but the protein is not.
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Nothing to worry about (yet) - outages due to people running too many scripts to scrape flybase. We just need everyone to follow @flybase.bsky.social 's guidelines: flybase.org/commentaries...
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Please apply here: www.ucl.ac.uk/work-at-ucl/...
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Informal enquiries welcome! Please get in touch for more information.