Characterization of the effects of an rpoC mutation which confers resistance to the Fst peptide TA system toxin.

Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion SD.
Journal of bacteriology (Impact Factor: 2.69). 10/2012; DOI: 10.1128/JB.01597-12
Source: PubMed

ABSTRACT Over-expression of the Fst toxin in Enterococcus faecalis strain OG1X leads to defects in chromosome segregation, cell division and, eventually, membrane integrity. The M7 mutant derivative of OG1X is resistant to most of these effects but shows a slight growth defect in the absence of Fst. Full genome sequencing revealed two differences between M7 and its OG1X parent. First, OG1X contains a frame-shift mutation that inactivates the etaR response regulator gene while M7 is a wild-type revertant at etaR. Second, the M7 mutant contains a missense mutation in the rpoC gene encoding the β' subunit of RNA polymerase. Mutagenesis experiments revealed that the rpoC mutation was primarily responsible for the resistant phenotype. Microarray analysis revealed that a number of transporters were induced in OG1X when Fst is over-expressed. These transporters were not induced in M7 in response to Fst and further experiments indicated that this had a direct protective effect on the mutant cells. Therefore, exposure of cells to Fst appears to have a cascading effect, first causing membrane stress and then potentiation of these effects by over-expression of certain transporters.

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