Coline Arnould

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 PERIOD proteins as regulators of TC-DSB repair by anchoring DSBs to the nuclear envelope, linking circadian rhythms to DNA repair mechanisms.

The paper identifies a new class of non-coding variants, dsbSNPs, that modulate DNA double-strand break frequency and are enriched in GWAS associations for complex diseases.

This study shows that CRISPR activation can rescue electrophysiological deficits in SCN2A haploinsufficiency by increasing the expression of the remaining functional allele in mice and human neurons.

This paper introduces ccMPRA, a method that combines Capture-C and MPRA to study promoter interactions and regulatory activity, identifying enhancers and silencers.

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.