Cohesin reshapes replication fork contacts to aid fork slowing and reversal.

Cohesin-mediated loop extrusion reorganizes replication fork contacts to promote fork slowing and reversal during replication stress, enhancing genome stability.

• Why it matters: Understanding how replication forks respond to stress is crucial for insights into genome integrity and cancer development, especially given the prevalence of cohesin mutations in tumors.
• What they did: The study used auxin-inducible degron, separation-of-function mutants, and a novel Micro-C-based Repli-C technique to analyze chromatin contacts at stressed replication forks, revealing cohesin accumulation and its role in fork regulation.
• The result: Findings demonstrate that cohesin's loop extrusion shifts fork contacts away from sister-fork coupling toward inter-replicon interactions, facilitating fork slowing and reversal, with implications for cancer therapy targeting cohesin functions.