Roles of DnaK and RpoS in starvation-induced thermotolerance of Escherichia coli

David Rockabrand, Kevin Livers, Tess Austin, Robyn Kaiser, Debra Jensen, Richard Burgess, Paul Blum

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


DnaK is essential for starvation-induced resistance to heat, oxidation, and reductive division in Escherichia coli. Studies reported here indicate that DnaK is also required for starvation-induced osmotolerance, catalase activity, and the production of the RpoS-controlled Dps (PexB) protein. Because these dnaK mutant phenotypes closely resemble those of rpoS (Σ38) mutants, the relationship between DnaK and RpoS was evaluated directly during growth and starvation at 30°C in strains with genetically altered DnaK content. A starvation-specific effect of DnaK on RpoS abundance was observed. During carbon starvation, DnaK deficiency reduced RpoS levels threefold, while DnaK excess increased RpoS levels nearly twofold. Complementation of the dnaK mutation restored starvation-induced RpoS levels to normal. RpoS deficiency had no effect on the cellular concentration of DnaK, revealing an epistatic relationship between DnaK and RpoS. Protein half-life studies conducted at the onset of starvation indicate that DnaK deficiency significantly destabilized RpoS. RpoH (σ32) suppressors of the dnaK mutant with restored levels of RpoS and dnaK rpoS double mutants were used to show that DnaK plays both an independent and an RpoS-dependent role in starvation- induced thermotolerance. The results suggest that DnaK coordinates sigma factor levels in glucose-starved E. coli.

Original languageEnglish (US)
Pages (from-to)846-854
Number of pages9
JournalJournal of bacteriology
Issue number4
StatePublished - Feb 1998

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology

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