Thomas Clouaire

The paper examines chromatin accessibility changes at DNA double-strand breaks (DSBs) in single cells, revealing resection-dependent remodeling and associated gene expression programs.

The paper identifies a novel chromatin compartment formed by ATM-dependent clustering of damaged TADs, which enhances DNA damage response but increases translocations.

The paper identifies TADs as functional units in DDR, showing cohesin-mediated loop extrusion contributes to {gamma}H2AX/53BP1 domain formation during DSB repair.

This study shows BLM promotes Homologous Recombination at DSBs in active chromatin but switches to Break-Induced Replication when R-loop dissolution is impaired, reducing cell viability.