Roles of DnaK and RpoS in Starvation-Induced Thermotolerance of Escherichia coli

Authors

David Rockabrand, University of Nebraska-Lincoln
Kevin Livers, University of Nebraska-Lincoln
Tess Austin, University of Nebraska-Lincoln
Robyn Kaiser, University of Nebraska-Lincoln
Debra Jensen, University of Wisconsin
Richard Burgess, University of Wisconsin
Paul H. Blum, University of Nebraska - LincolnFollow

Document Type

Article

Date of this Version

1998

Citation

Journal of Bacteriology, Feb. 1998, p. 846–854 Vol. 180, No. 4

Comments

Copyright © 1998, American Society for Microbiology

Abstract

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 (o³⁸) 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 (s32) 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.