期刊
MOLECULAR CELL
卷 77, 期 4, 页码 723-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2019.12.010
关键词
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资金
- UC San Diego Quantitative and Integrative Biology training grant [NIH T32 GM127235]
- NIH [T32 HL007444, T32 GM007752, F31 CA236405, K01 DK116917, P30 DK063491, R01 GM129245, R01 ES027595, S10 OD020025]
- Herchel Smith Graduate Research Fellow
- NIH/NIAID [R01AI018045, R01AI026289]
- Ri-chard and Susan Smith Foundation
- Parker Institute for Cancer Immunotherapy
- Ludwig Institute for Cancer Research
- University of California, San Diego
Bacteria possess an array of defenses against foreign invaders, including a broadly distributed bacteriophage defense system termed CBASS (cyclic oligonucleotide-based anti-phage signaling system). In CBASS systems, a cGAS/DncV-like nucleotidyltransferase synthesizes cyclic di- or tri-nucleotide second messengers in response to infection, and these molecules activate diverse effectors to mediate bacteriophage immunity via abortive infection. Here, we show that the CBASS effector NucC is related to restriction enzymes but uniquely assembles into a homotrimer. Binding of NucC trimers to a cyclic tri-adenylate second messenger promotes assembly of a NucC homohexamer competent for non-specific double-strand DNA cleavage. In infected cells, NucC activation leads to complete destruction of the bacterial chromosome, causing cell death prior to completion of phage replication. In addition to CBASS systems, we identify NucC homologs in over 30 type III CRISPR/Cas systems, where they likely function as accessory nucleases activated by cyclic oligoadenylate second messengers synthesized by these systems' effector
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