Clara Basto, PhD student of the team of Gerard Mazón/Eric Le Cam under the supervision of Pauline Dupaigne has been awarded the « Prix coup de coeur du Jury » for her talk during the 29th « Journées Jeunes Chercheurs de la Fondation ARC ».
Masato Kanemaki from the University of Tokyo. (NEW TIME!)
Friday, 17 October at 10:30 at Salle Roger Monier
AAPG 2026 of the ANR (1st phase) closing on 14th October
OK-seq is a technique that sequences strand-specific Okazaki fragments to map replication initiation and termination in mammalian genomes. It quantifies fork directionality, revealing replication dynamics at high resolution. N. Petryk team contributes to this work to provide detailed protocols for OK-seq in human cells and yeast, alongside bioinformatics pipelines.
The 7th German-French DNA repair meeting will be held this November 5th-7th in Paris. The unit is this time involved as hosting/organizing committee of the meeting. We will wellcome you soon!
This work, led by P. Laplante in Kannouche’s team, shows how mismatch repair deficiency causes high mutation rates and microsatellite instability (MSI-H), linked to immune infiltration and immunotherapy response.
A syngeneic MSI breast cancer mouse model with Msh2 knockout showed reduced metastasis and immune gene enrichment. Aggressive hybrid epithelial-mesenchymal signatures appeared only in metastatic MSI-H tumors. Immature myeloid cells at tumor sites suggest unique immune responses beyond T-cell activation in MMR deficiency.
La retraite de l’unité aura lieu le 16 Octobre 2025 à la cité U (Fondation Deutsch de la Meurthe). RDV à 8:45!
Fondation Deutsch de la Meurthe au CIUP (RER cité U).
Attention ! :
– L’Accès Piéton se fera par le 37 Boulevard Jourdan, 75014 PARIS
– L’Accès voiture se fera par les 27/29/31 Boulevard Jourdan 75014 PARIS
The Gavet team developed a FRET-based sensor to specifically monitor Chk1 activity during replication stress (RS).
Basal Chk1 activity during S phase depends on replication origin firing, with RS triggering stepwise Chk1 over-activation that delays S-phase.
Chk1 is inactivated upon replication completion but reactivates in some G2 cells to block premature mitosis.
Cells can override active Chk1 signaling to enter mitosis, revealing checkpoint adaptation.
Beatrice Rondinelli co-authors a study revealing that pediatric high-grade gliomas (pHGG) with H3.3 mutations exhibit aberrant DNA repair promoting genome instability. Their findings suggest new therapeutic targets for treating H3.3 mutant pHGG.
This article is a collaboration of the Kannouche team with the Gustave Roussy’s team of S. Nikolaev. Xeroderma pigmentosum (XP) is caused by mutations in NER genes or DNA polymerase η, leading to a greatly increased skin cancer risk.
Analysis of 38 XP skin cancer genomes reveals that NER activity drives mutation rate variability and that transcription-coupled NER reduces intergenic mutations.
The findings clarify the genetic basis of skin cancer risk in XP.