期刊
SCIENCE
卷 369, 期 6505, 页码 823-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaw6421
关键词
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资金
- SNF [BSSGI0-155984, 31003A_159836]
- Gebert Ruf Foundation [GRS-059_14]
- NCCR Chemical Biology
- ERC [804933, 724022, 714609]
- Long-Term EMBO Fellowship [ALTF 203-2016]
- Swiss National Science Foundation (SNF) [31003A_159836] Funding Source: Swiss National Science Foundation (SNF)
- European Research Council (ERC) [714609, 804933, 724022] Funding Source: European Research Council (ERC)
The appearance of DNA in the cytosol is perceived as a danger signal that stimulates potent immune responses through cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS). How cells regulate the activity of cGAS toward self-DNA and guard against potentially damaging autoinflammatory responses is a fundamental biological question. Here, we identify barrier-to-autointegration factor 1 (BAF) as a natural opponent of cGAS activity on genomic self-DNA. We show that BAF dynamically outcompetes cGAS for DNA binding, hence prohibiting the formation of DNA-cGAS complexes that are essential for enzymatic activity. Upon acute loss of nuclear membrane integrity, BAF is necessary to restrict cGAS activity on exposed DNA. Our observations reveal a safeguard mechanism, distinct from physical separation, by which cells protect themselves against aberrant immune responses toward genomic DNA.
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