Sébastien Britton

The @RoukosVassilis lab led a new and detailed study of Topoisomerase II contribution to #3Dgenome folding in human cells and in different cell cycle phases -- my group and the @MundlosLab contributed analyses/data. The paper is now published in @MolecularCell ...1/n

‼️highlight alert‼️ Thanks @CNRSchimie for highlighting this @icmub work done in collaboration with @agranzhan @institut_curie @SebBritton1 @IpbsToulouse Nicolas Chéron @Chimie__ENS and Lukas Trantirek @CEITEC_Brno

Group leader in Infection Biology @IpbsToulouse The IPBS-Toulouse recruits a Group leader in Infection Biology jobrxiv.org/job/institute-… #ScienceJobs #job jobrxiv.org/job/institute-…

If you are a bright Ph.D. student working outside France around our research theme ipbs.fr/fr/mecanismes-… @IpbsToulouse , here is a chance for you to contact us to apply for the open Excellence Eiffel Fellowship univ-tlse3.fr/venir-a-l-univ… contact us before October 20th, 2024 !!

Come join us as a postdoc in the JaJa lab at the Netherlands Cancer Institute if you are interested in the molecular mechanisms underlying telomere maintenance by ALT and in findings ways how to target ALT in pediatric cancer treatment.nki.nl/careers-study/…

Our lab, @IpbsToulouse is looking for a motivated research engineer with fluency in French and English, interested in our research theme, ipbs.fr/fr/mecanismes-…. Please apply here: emploi.cnrs.fr/Gestion/Offre/… Please retweet 🙏

#ResultatScientifique 🔎 | Du nouveau sur la régulation des mécanismes de réparation de l’ADN 🤝 @CNRS @CNRS_Toulouse @UT3PaulSabatier @IpbsToulouse ✍️ @SebBritton1 📕 @CellReports | buff.ly/3ACUTAR buff.ly/475vCeD

1/7 Our latest preprint is out! 🚨 @Sour_Agrawal , @xiuhua_linwisc , @viveksusvirkar et al. discover human RPA is a critical telomerase processivity factor essential for telomere maintenance. This reshapes our understanding of human telomerase regulation. biorxiv.org/content/10.110…

Have you ever wondered why some cell lines are easy to edit with CRISPR-mediated gene editing, while others are more difficult? Our paper is now online and offers an interesting answer: nature.com/articles/s4158…

Our latest manuscript on a new cell cycle dependent control of dna repair. Started from a high resolution crispr screen of #ubiquitin system after IR: check table S2! Also substrates of cyclin f through motif search! science.org/doi/10.1126/sc…

Optimized methods for mapping DNA double-strand-break ends and resection tracts and application to meiotic recombination in mouse ... biorxiv.org/cgi/content/sh… #biorxiv_genomic

Happy to share a publication from the lab demonstrating that 53BP1 loss is a positive predictive biomarker for immune checkpoint blockade efficacy, with important implications for the treatment of PARPi-resistant ovarian and pancreatic cancers! nature.com/articles/s4146…

🔥🔥🔥 PREPRINT 🔥🔥🔥 Wanna know how your favorite gene affects double-strand break repair outcome/CRISPR-Cas9 gene editing? Check this out! ⬇️ #REPAIRome biorxiv.org/content/10.110…

@ocalvayrac 😊 Thanks Olivier!

In vitro, multiple #DNA_repair proteins Ku load from DNA ends on linear DNA, eventually covering it. Yet, in cells, only one Ku is found per DNA end at double-strand breaks. What restricts Ku entry on chromatin? doi.org/10.1016/j.celr…

@AgneseCristini Thanks Agnese!

@SebBritton1 Congrats !!

@DrBillonPierre Thank you Pierre !😊@MadeleineBsrt did a terrific work!

@SebBritton1 Beautiful work, Seb! 👌Glad to see it published 😍

Really proud of this one! Thanks to our collaborators @JoeLoparo lab for single-molecule experiments in Xenopus egg extracts, the kind reviewers, @CellReports for the pleasant publishing experience, and our funders @Liguevscancer31 @laliguecancer @FRM_officiel

In this work, we identify the main barriers to Ku accumulation in chromatin: DNA-PKcs structurally retains Ku at DNA ends. If Ku enters chromatin, it is removed by a neddylation/FBXL12-dependent process. In S-phase, DNA end resection can remove Ku, even in excess.

These mechanisms are crucial: transcription is inhibited locally by Ku without DNA-PKcs, and FBXL12 is vital for the fitness of DNA-PKcs deficient cells. Our findings highlight the complex regulation of Ku, necessary to maintaining genome integrity.