I am not surprised since the SNSF also took similar measures - seems to be seen as the less damaging way to deal with budgetary restrictions. Very annoying, but in the end we should blame the angry little white men in charge of certain large countries and the systems allowing them to stay in power
Congraaaats Can ! Your passion for science paid off nicely with this beautiful piece of work !
Join us at the LS2 #Theory #across #Biology chalk talk symposium! 12 June 2026 in Bern, CH. @lifesciswitzerland.bsky.social
No movies that fail, no Mac to PC issues. Only the best ideas and exchange across biology from evolution and ecology to physics of life.
meetings.ls2.ch/theory-acros...
Monthly median Received to Accepted time (days) at Nature Genetics
That’s a killer argument, how could one imagine cycling without eating
skyr
Do we grow wiser as we age?
I spent 15+ years chasing glam journals, wasting time and energy (and frustrating my team and co-authors).
I don’t want to wake up at 70 and realize my life went into convincing a few editors my work was trendy enough.
Enough. I’ll try to be smarter.
Non-science post - Any plans for Easter ? If not, come join us in Evian 🇫🇷 on 4.4. for the piano marathon !
My menu: Brahms : Rhapsodie op.79 n°1, Schumann : 2 pieces from Fantaisiestücke op. 12, Chopin : Ballade n°4 & Mazurka op.59 n°2 info 👇
marathondupiano.com
www.youtube.com/watch?v=ya7M...
The Evolution of Academia
Email spam in 2026 is so out of control that it feels like smashing nagging mosquitoes on a hot summer night
Demons - Dostoïevski
Yes I agree !
Yep, we also encountered the same issues - motif of the TF we ChIP only showing up in 30-40% of peaks, and other TF motifs - typically Klfs that are biased towards promoters - showing up more frequently
Yes ! But still, I am worried that the approaches most of us are using are even further from providing realistic, quantitative maps of where TFs bind in the genome than we previousy thought
Also the very strong discrepancy with ChIP-seq and CUT&RUN is rather sobering to the field
Wondering whether this relatively "extreme" finding is also related to the fact that the TFs studied bind more to promoters (typically highly accessible), rather than enhancers ? Would seem intuitive to me that promoter binding depends relies less on specific motif recognition, but I might be wrong
Very interesting work from on the role of IDRs in DNA binding specificity - in the cases studied here, the DBD plays almost no role 😮. www.science.org/doi/epdf/10....
Thanks so much Silvia 🙏
TFs search are governed by many parameters, what about electrostatic forces? @simsakong.bsky.social led a multi-scale study on Sox2 revealing how electrostatic interactions influence its search. In close collaboration with @davidsuter.bsky.social. Congratulations Sim 🎉
www.nature.com/articles/s41...
Huge thank you to the protein production, flow cytometry, bioimaging and genomics core facilities without whom this work would not have been possible 🙏🙏🙏🙏
In addition, Sim found that the more positively-charged DBD-flanking regions increase not only TF search efficiency but also pioneer activity, explaining why Sox2 is particularly potent in opening chromatin as compared to Sox17.
Sim found that the more positively-charged flanking regions of Sox2 boost search efficiency compared to Sox17. On naked DNA, Sox2 displays superior target recognition during sliding, while in chromatin, stronger interactions with nucleosomes help Sox2 access tightly packed DNA.
How do electrostatic forces impact TF search ? In joint effort with @beatfierz.bsky.social , tour-de-force from @simsakong.bsky.social who single-handedly combined in vitro SPT on DNA & chromatin, in cellulo SPT, ChIP-seq and ATAC-seq www.nature.com/articles/s41...
Waou ! Fabulous documentary, so much deserved !
Submitting to Nature Friend instead of Nature
Big thanks to the genomics, bioimaging, flow cytometry and biomolecular screening core facilities of EPFL and to the SNSF for funding this project.
Many of the TFs targeted by H2A.Z at the transcriptional level are the same that are blocked in their binding by SRCAP.
H2A.Z and SRCAP thus work together in restricting both expression and activity of lineage-specific TFs, thereby gatekeeping the pluripotent state of mouse ES cells.
Turns out that H2A.Z restricts transcriptional activation of lineage-specific genes. While SRCAP deposits H2A.Z on chromatin, it also showed a surprising H2A.Z-independent function by blocking pioneer transcription factor binding to nucleosomes by steric hindrance.
Armelle and coworkers (big thanks in particular to Enes Ugur, Heinrich Leonhardt, Susanna Dalla Longa, @gebhardtlab.bsky.social & Cédric Deluz) combined rapid SRCAP degradation, a catalytically dead SRCAP mutant, omics and single molecule imaging to dissect the specific functions of H2A.Z and SRCAP
