期刊
NUCLEIC ACIDS RESEARCH
卷 45, 期 17, 页码 9976-9989出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkx656
关键词
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资金
- National Natural Science Foundation of China [31500050, 31270786]
- Shandong Academy of Medical Sciences
- Department of Health and Family-plan Bureau, Shandong Province [2016WS0525, 2015WS0188]
- Shandong Academy of Medical Sciences [2015-27]
- Shandong Provincial College of Traditional Chinese Medicine Antiviral Collaborative Innovation Center [XTCX2014B01-05]
- National Science and Technology Major Special Project of China [2014ZX09509-001001008]
- Shandong Academy of Medical Sciences
Salmonella reduces flagella biogenesis to avoid detection within host cells by a largely unknown mechanism. We identified an EAL-like protein STM1697 as required and sufficient for this process. STM1697 surges to a high level after Salmonella enters host cells and restrains the expression of flagellar genes by regulating the function of flagellar switch protein FlhD(4)C(2), the transcription activator of all other flagellar genes. Unlike other anti-FlhD(4)C(2) factors, STM1697 does not prevent FlhD(4)C(2) from binding to target DNA. A 2.0 angstrom resolution STM1697-FlhD structure reveals that STM1697 binds the same region of FlhD as STM1344, but with weaker affinity. Further experiments show that STM1697 regulates flagella biogenesis by restricting FlhD(4)C(2) from recruiting RNA polymerase and the regulatory effect of STM1697 on flagellar biogenesis and virulence are all achieved by interaction with FlhD. Finally, we describe a novel mechanism mediated by STM1697 in which Salmonella can inhibit the production of flagella antigen and escape from the host immune system.
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