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Barrier-to-autointegration factor protects against the cGAS-STING response to chromatin bridges

Laura Chastant1, Karine Normandin1, Firas El-Mortada2

  • 1Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada.

Plos Genetics
|June 3, 2026
PubMed

Insights

Mitotic defects can trigger innate immune responses. This study reveals that destabilized chromatin bridges, not micronuclei, are key activators of the cGAS-STING pathway following cell division errors.

Area of Science:

  • Cellular biology
  • Immunology
  • Genetics

Background:

  • Cellular damage and stress can activate innate immune responses through self-DNA.
  • Micronuclei from mitotic defects are implicated in activating the cGAS-STING pathway, leading to inflammation.
  • The precise role of micronuclei versus other mitotic defects in this activation remains unclear.

Purpose of the Study:

  • To investigate the role of post-mitotic defects in inducing innate immune responses.
  • To compare the effects of Spindle-Assembly Checkpoint inhibition and BAF inactivation on the cGAS-STING pathway.
  • To elucidate the specific structures that activate the cGAS-STING pathway following mitotic errors.

Main Methods:

  • Inhibition of the Spindle-Assembly Checkpoint using MPS1 inhibitors.
  • Interference with nuclear reassembly via BAF inactivation.
  • Analysis of cGAS-STING pathway activation and associated cellular structures.

Main Results:

  • Combining MPS1 inhibition and BAF inactivation synergistically enhanced the cGAS-STING response.
  • This enhancement was not linked to increased micronucleation or lobulation.
  • The response correlated with an increase in destabilized chromatin bridges that recruit cGAS.

Conclusions:

  • BAF stabilizes chromatin bridges, preventing their conversion into cGAS-activating structures.
  • Destabilized chromatin bridges, rather than micronuclei, are potent inducers of the cGAS-STING pathway following mitotic defects.
  • This research clarifies how the innate immune system detects errors during cell division.

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