Web of Science: 18 cites, Scopus: 22 cites, Google Scholar: cites,
Critical role for a promoter discriminator in RpoS control of virulence in Edwardsiella piscicida
Yin, Kaiyu (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Guan, Yunpeng (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Ma, Ruiqing (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Wei, Lifan (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Liu, Bing (Universitat Autònoma de Barcelona. Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí")
Liu, Xiaohong (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Zhou, Xiangshan (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Ma, Yue (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Zhang, Yuanxing (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Waldor, M.K. (Harvard Medical School)
Wang, Qiyao (East China University of Science and Technology. State Key Laboratory of Bioreactor Engineering)
Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular

Data: 2018
Resum: Edwardsiella piscicida is a leading fish pathogen that causes significant economic loses in the aquaculture industry. The pathogen depends on type III and type VI secretion systems (T3/T6SS) for growth and virulence in fish and the expression of both systems is controlled by the EsrB transcription activator. Here, we performed a Tn-seq-based screen to uncover factors that govern esrB expression. Unexpectedly, we discovered that RpoS antagonizes esrB expression and thereby inhibits production of E. piscicida's T3/T6SS. Using in vitro transcription assays, we showed that RpoS can block RpoD-mediated transcription of esrB. ChIP-seq- and RNA-seq-based profiling, as well as mutational and biochemical analyses revealed that RpoS-repressed promoters contain a -6G in their respective discriminator sequences; moreover, this -6G proved critical for RpoS to inhibit esrB expression. Mutation of the RpoS R99 residue, an amino acid that molecular modeling predicts interacts with -6G in the esrB discriminator, abolished RpoS' capacity for repression. In a turbot model, an rpoS deletion mutant was attenuated early but not late in infection, whereas a mutant expressing RpoSR99A exhibited elevated fitness throughout the infection period. Collectively, these findings deepen our understanding of how RpoS can inhibit gene expression and demonstrate the temporal variation in the requirement for this sigma factor during infection.
Drets: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original. Creative Commons
Llengua: Anglès
Document: Article ; recerca ; Versió publicada
Matèria: Animals ; Aquaculture ; Bacterial Proteins ; Edwardsiella ; Enterobacteriaceae Infections ; Fish Diseases ; Flatfishes ; Gene Expression Regulation, Bacterial ; Promoter Regions, Genetic ; Protein Binding ; Sigma Factor ; Virulence
Publicat a: PLoS pathogens, Vol. 14 issue 8 (2018) , art. e1007272, ISSN 1553-7374

DOI: 10.1371/journal.ppat.1007272
PMID: 30169545


28 p, 7.6 MB

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Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut de Biotecnologia i de Biomedicina (IBB)
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 Registre creat el 2020-06-22, darrera modificació el 2021-08-01



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