PerspectiveImmunology

DNA sensor in standby mode during mitosis

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Science  19 Mar 2021:
Vol. 371, Issue 6535, pp. 1204-1205
DOI: 10.1126/science.abg7422

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Summary

Pathogen sensing in innate immunity relies on receptors that must be efficient and precise. To achieve this, cells express various signaling receptors that bind microbial structures, which are absent in the host. In addition, a fascinating mechanism of pathogen sensing is based on the recognition of double-stranded DNA (dsDNA). Coupling such a universal signal to the execution of immune defense not only enables protection against a broad spectrum of pathogens but also allows for the identification of damaged host cells. However, activating immunity to self-DNA can have fatal consequences for the host. What mechanisms guide the critical decision about whether to respond to a DNA molecule? On page 1221 of this issue, Li et al. (1) report that cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS)—a major host sensor for dsDNA—exploits phosphorylation and chromatin tethering during mitosis, which abolishes its activity on host genomic DNA.

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