BAF protein shown to suppress cGAS-STING innate immune activation at chromatin bridges in PLOS Genetics study

A study published on 3 June 2026 in *PLOS Genetics* by Laura Chastant, Karine Normandin, Firas El-Mortada, Marc J. Servant, Vincent Archambault and colleagues at Université de Montréal investigates how cells avoid misfiring the cGAS-STING innate immune pathway in the presence of chromatin bridges — aberrant DNA structures that can form when chromosomes fail to segregate correctly during cell division.

The cGAS-STING pathway is a central sensor of cytosolic DNA, normally activated by viral or bacterial DNA but capable of being triggered by displaced self-DNA, including DNA contained in micronuclei formed after mitotic errors. Whether cGAS-STING activation during mitotic defects is primarily a consequence of micronuclei per se or of other concurrently arising structural aberrations, such as chromatin bridges, had remained unclear.

The authors demonstrate that barrier-to-autointegration factor (BAF), a chromatin-associated protein, acts as a suppressor of cGAS-STING activation specifically at chromatin bridges, preventing IRF3-dependent proinflammatory transcription. The findings help delineate the circumstances under which genomic instability escalates into inflammation — a distinction with potential relevance for understanding the inflammatory tumour microenvironment and conditions characterised by sterile inflammation driven by self-DNA sensing.

The study is peer-reviewed basic research published in an open-access journal. It does not present clinical data or propose any diagnostic or therapeutic application.