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Faulty replication can sting

Inappropriate cellular inflammation can cause disease. It emerges that the protein SAMHD1 prevents the release of newly replicated DNA from the nucleus, blocking an undesirable pro-inflammatory response.
  1. Madzia P. Crossley

    1. Madzia P. Crossley is in the Department of Chemical & Systems Biology, Stanford University, Stanford, California 94305, USA.

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  2. Karlene A. Cimprich

    1. Karlene A. Cimprich is in the Department of Chemical & Systems Biology, Stanford University, Stanford, California 94305, USA.

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Cells need to distinguish between their own DNA and that of viruses. To solve this problem, plant, fungal and animal cells store their DNA in the nucleus, and respond to DNA in the cytoplasm by activating an inflammatory response. However, under certain abnormal circumstances, host-cell DNA can also accumulate in the cytoplasm, triggering inappropriate inflammation. In a paper in Nature, Coquel et al.1 define a role for the protein SAMHD1 in preventing this cytoplasmic host-DNA build-up. The authors’ findings have implications for immune disease and cancer.

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Nature 557, 34-35 (2018)

doi: https://doi.org/10.1038/d41586-018-02804-6

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