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Phenotypic heterogeneity and temporal expression of the capsular polysaccharide in S taphylococcus aureus
Author(s) -
George Shilpa E.,
Nguyen Tran,
Geiger Tobias,
Weidenmaier Christopher,
Lee Jean C.,
Liese Jan,
Wolz Christiane
Publication year - 2015
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.13174
Subject(s) - biology , quorum sensing , effector , repressor , phenotype , virulence , phase variation , population , gene expression , gene , microbiology and biotechnology , regulation of gene expression , autoinducer , staphylococcus aureus , bacteria , genetics , demography , sociology
Summary Bacteria respond to ever‐changing environments through several adaptive strategies. This includes mechanisms leading to a high degree of phenotypic variability within a genetically homogeneous population. In S taphylococcus aureus , the capsular polysaccharide ( CP ) protects against phagocytosis, but also impedes adherence to endothelial cells and/or matrix proteins. We analysed the regulation of core biosynthesis genes ( capA‐ P ) necessary for CP synthesis using single‐cell assays (immunofluorescence and promoter‐activity). In persistent human carriers, we found a distinct subpopulation of nasal S . aureus to be CP positive. In vitro , cap expression is also heterogeneous and strongly growth‐phase dependent. We asked whether this peculiar expression pattern (earlyOff/lateHeterogen) is orchestrated by the quorum system A gr. We show that the A gr‐driven effector molecule RNAIII promotes cap expression largely via inactivation of the repressor R ot. High NaCl , deletion of CodY or Sae also resulted in higher cap expression but did not change the earlyOFF/lateHeterogen expression pattern. Activity of the quorum system itself is largely homogenous and does not account for the observed heterogeneity of cap expression or the strictly growth phase dependent expression. Our findings are in contrast to the prevailing view that quorum sensing is the main driving force for virulence gene expression when bacterial cell densities increase.