Abstract
A mutation in the cell division gene ftsK causes super-induction of sigma(70)-dependent stress defense genes, such as uspA, during entry of cells into stationary phase. In contrast, we report here that stationary phase induction of sigma(S)-dependent genes, uspB and cfa, is attenuated and that sigma(S) accumulates at a lower rate in ftsK1 cells. Ectopic overexpression of rpoS restored induction of the rpoS regulon in the ftsK mutant, as did a deletion in the recA gene. Thus, a mutation in the cell division gene, ftsK, uncouples the otherwise coordinated induction of sigma(S)-dependent genes and the universal stress response gene, uspA, during entry into stationary phase.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism*
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Cyclopropanes / metabolism
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Escherichia coli / genetics
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Escherichia coli / growth & development*
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Escherichia coli Proteins
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Fatty Acids / metabolism
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Gene Deletion
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Gene Expression Regulation, Bacterial*
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Membrane Proteins / genetics*
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Membrane Proteins / metabolism
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Mutation*
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Rec A Recombinases / genetics
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Sigma Factor / genetics
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Sigma Factor / metabolism*
Substances
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Bacterial Proteins
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Cyclopropanes
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Escherichia coli Proteins
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Fatty Acids
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FtsK protein, E coli
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Membrane Proteins
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Sigma Factor
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cyclopropane fatty acids
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sigma factor KatF protein, Bacteria
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cyclopropane
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Rec A Recombinases