A new study shows cohesin reshapes replication fork contacts to slow or reverse fork progression, preventing DNA damage and contributing to genome stability.

Beyond its known roles in holding sister chromatids and organizing genome structure, cohesin rapidly localizes to replication-stress sites to stabilize newly replicated DNA and preserve genome integrity.

The findings could influence precision oncology, as many cancer therapies induce replication stress; targeting cohesin’s protective mechanism may improve tumor cell killing while sparing healthy cells, and cohesin mutations in cancers may affect treatment responses.

The work was a collaboration between IMCR (University of Zurich) and CNIO (Ana Losada’s group), led by Daniel González with key contributions from Daniel Giménez and others, using a novel genomic approach to map 3D organization of newly replicated DNA and microscopy data.

Researchers from the University of Zurich and CNIO report a new role for cohesin in protecting genetic information during DNA replication and cell division, as published in Nature.

Publication: González-Acosta, D., et al. Cohesin reshapes replication fork contacts to aid fork slowing and reversal, Nature (2026); DOI: 10.1038/s41586-026-11034-0.

Cohesin’s protective action includes preventing activation of the restart factor Primpol, reducing potential mutations during replication stress.