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Virulence gene repression promotes Listeria monocytogenes systemic infection

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  • معلومة اضافية
    • Contributors:
      Lallemant, Christopher; Instituto de Investigação e Inovação em Saúde; Instituto de Investigação e Inovação em Saúde (I3S); Universidade do Porto = University of Porto; Group of Molecular Microbiology; Instituto de Biologia Molecular e Celular (IBMC); Interactions Bactéries-Cellules (UIBC); Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM); Cell Biology of Bacterial Infections; FEDER - Fundo Europeu de Desenvolvimento Regional funds through the NORTE 2020 - Norte Portugal Regional Operational Programme, Portugal 2020 Portuguese funds through FCT - Fundacao para a Ciencia e a Tecnologia/Ministerio da Ciencia, Tecnologia e Ensino Superior NORTE-01-0145-FEDER-030020 PTDC/SAU-INF/30020/2017FCT through FCT/MEC - QREN SFRH/BD/89542/2012SFRH/BD/29314/2006POPH (Programa Operacional Potencial Humano) FCT Investigator program (COMPETE) FCT Investigator program (POPH) FCT Investigator program (FCT); European Project: 670823,H2020,ERC-2014-ADG,BacCellEpi(2015); Universidade do Porto; Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)
    • بيانات النشر:
      Informa UK Limited, 2020.
    • الموضوع:
      2020
    • نبذة مختصرة :
      The capacity of bacterial pathogens to infect their hosts depends on the tight spatiotemporal regulation of virulence genes. The Listeria monocytogenes (Lm) metal efflux pump repressor CadC is highly expressed during late infection stages, modulating lipoprotein processing and host immune response. Here we investigate the potential of CadC as broad repressor of virulence genes. We show that CadC represses the expression of the bile salt hydrolase impairing Lm resistance to bile. During late infection, in absence of CadC-dependent repression, the constitutive bile salt hydrolase expression induces the overexpression of the cholic acid efflux pump MdrT that is unfavorable to Lm virulence. We establish the CadC regulon and show that CadC represses additional virulence factors activated by σB during colonization of the intestinal lumen. CadC is thus a general repressor that promotes Lm virulence by down-regulating, at late infection stages, genes required for survival in the gastrointestinal tract. This demonstrates for the first time how bacterial pathogens can repurpose regulators to spatiotemporally repress virulence genes and optimize their infectious capacity.
    • File Description:
      application/pdf
    • ISSN:
      1949-0984
      1949-0976
    • الرقم المعرف:
      10.1080/19490976.2020.1712983
    • Rights:
      CC BY NC
    • الرقم المعرف:
      edsair.doi.dedup.....6cd4e2bbe4bc287351af4f1b7769dcca