Your immune system fights invaders with tools evolved from a tamed genomic invader

Мы, учёные, восхищались людским гением. А теперь ИИ строчит стихи, а наш удел? Крутить гайки (или пыхтеть за лабораторным столом). Будущее человечества — не поэзия, а сантехника! P.S. Твит написан ИИ

As scientists, we marveled at human creativity. Now AI’s writing poems, and our last gig? Wielding a wrench (or toiling at the bench). Humanity’s future is less poetic, more pipe-fixing. P.S. Tweet written by AI

looking forward to sharing my PhD work with @AlexeiAravin @Caltech at #Dros25 tonight & meeting old and new friends throughout the fly meeting 😀

This is THE problem. Overt fraud is (hopefully) rare, but this is not. Of course, it is not that glamour journals are to be blamed for this exclusively. Many scientists are more than happy to play this game

🎯🎯🎯

A culture that "reward[s] 'winners' (postdocs who generate favorable results) and marginalizes 'losers' (postdocs who struggle to generate such data)” leads to 20 years of "fudging of results [in] labs at three separate institutions".

I see the peer-review and editorial process - especially in so-called top-tier journals - as a great impediment to doing good science.

A great review of antiphage systems – the topic which is exploded over the last few years. However, only a subset of pAgos antiphage mechanisms are shown in this figure. Unlike catalytically inactive short pAgos, active pAgos directly attack invading phages cleaving their DNA.

Thus, different short pAgo use distinct molecular mechanisms, but all act as abortive infection systems that trigger cell death when it is infected by foreign elements.

Other short pAgos form complexes with a distinct nuclease. Target recognition unleashes the nuclease activity causing indiscriminate collateral cleavage of DNA and RNA. Activation of such pAgo occurs during phage infection and leads to cell death. https://t.co/NFSBfR3MYn /3

Some short pAgo form complexes with TIR or SIR2 proteins. Recognition of the target by pAgo activates NADase activity of TIR or SIR2 domain. NAD depletion causes cell death. Beautiful papers from Siksnys and Swarts labs: https://t.co/wi3yYELWdE https://t.co/fGyKUygF53 /2

The new story from the world of prokaryotic Argonautes. Reminder: Argonaute is the only defense system present in all domains of life! A large fraction of Argonautes in prokaryotes is so-called short Agos that lack catalytic activity. How do they work? /1

woke up to a Dispatch article by Mark Van Doren and Caitlin Pozmanter @CaiPoz highlighting our recent work @CurrentBiology 😍 it is the mood boost that one needs on this gray, rainy Monday in LA! https://t.co/JqB59SQLFp

Happy to share that our work with @AlexeiAravin exploring the ovarian SUMOylome by proteomics is now published online in @CellGenomics https://t.co/yKx0HnJCv6 🎉 1/2

- Unlike KAP-1 which promotes its own SUMOylation, Bonus relies on a separate SUMO-ligase . Although TIF1 proteins are SUMOylated in both insects and mammals, both the SUMOylation mechanisms and sites of modification are different, suggesting it has developed independently /7

- Bonus is modified by SUMO at a single site and this modification is essential for its repressive activity. Lack of SUMOylation causes the dissociation of Bonus from chromatin and its accumulation in distinct nuclear granules. /6

- Bonus acts as a potent transcriptional repressor when recruited to chromatin and this repression associates with an accumulation of repressive histone marks. /5

- In the germline, Bonus represses ectopic expression of genes that are normally expressed in somatic tissues, but it is not involved in the repression of transposons. /4

flies have a TIF1 homolog called Bonus, but do not have any KRAB proteins. It turned out that Bonus is quite different from KAP1: - Bonus is essential for female germline development and fertility, including the maintenance and development of germline stem cells. /3