Role of the Escherichia coli FadR Regulator in Stasis Survival and Growth Phase-Dependent Expression of the uspA, fad, and fab Genes

Authors

Anne Farewell, Lund University
Alfredo A. Diez, Lund University
Concetta C. DiRusso, University of Nebraska-LincolnFollow
Thomas Nyström, Lund University

Document Type

Article

Date of this Version

1996

Citation

Journal of Bacteriology, Nov. 1996, p. 6443–6450 Vol. 178, No. 22

Comments

Copyright 1996, American Society for Microbiology

Abstract

The increased expression of the uspA gene of Escherichia coli is an essential part of the cell’s response to growth arrest. We demonstrate that stationary-phase activation of the uspA promoter is in part dependent on growth phase-dependent inactivation or repression of the FadR regulator. Transcription of uspA is derepressed during exponential growth in fadR null mutants or by including the fatty acid oleate in the growth medium of FadR1 cells. The results of DNA footprinting analysis show that FadR binds downstream of the uspA promoter in the noncoding region. Thus, uspA is a member of the fadR regulon. All the fad-lacZ fusions examined (fadBA, fadL, and fadD) are increasingly expressed in stationary phase with kinetics similar to that of the increased expression of uspA. In contrast, b-galactosidase levels decrease during stationary phase in a fabA-lacZ lysogen,

consistent with the role of FadR as an activator of fabA. The growth phase-dependent increased and decreased transcription of fad genes and fabA, respectively, is dependent on the status of the fadR gene. Cells carrying a mutation in the FadR gene (fadRS219N) that makes it nonderepressible exhibit a weak stationary-phase induction of uspA and fad genes. In addition, cells carrying fadRS219N survive long-term stasis poorly, indicating that FadR-dependent alterations in fatty acid metabolism are an integral and important part of the adaptation to stationary phase.