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Research Papers

Isolation and characterization of an Escherichia coli mutant defective in resuming growth after starvation.

Department of Biology, Texas A&M University, College Station 77843-3258.

Abstract

To understand the mechanisms that allow the enteric bacterium Escherichia coli to make the transitions between growth and stationary phase and to maintain cell viability during starvation, we have looked for mutants defective in stationary-phase survival (a Sur- phenotype). In this paper we describe a conditional E. coli mutant, surB1, that grows normally and remains viable during stationary phase but is unable to exit stationary phase and resume aerobic growth at high temperature. Thus, the surB gene product is not required for cell survival per se but, rather, it is required for starved cells to reinitiate growth under restrictive conditions. Once growth has started, SurB function is no longer required. Mutant cells sense and respond to fresh medium but appear to arrest growth before the first cell division. The surB gene was mapped to 19.5 min on the E. coli chromosome, cloned, and sequenced. The surB gene product is predicted to be an integral membrane protein with multiple membrane-spanning regions and is homologous to the ATP-binding cassette (ABC) family of transporters, a large family of transport proteins found in both prokaryotic and eukaryotic cells. An open reading frame, designated ybjA, was found immediately upstream of surB and may be in an operon with surB. The predicted ybjA gene product is also homologous to the ABC transporter family and SurB and YbjA may function together in a common transport pathway. Either surB or ybjA may be the same gene as cydC, a gene described previously whose function is needed for the production of functional cytochrome d oxidase complexes. Consistent with this prediction, surB1 mutant cells were found to lack functional cytochrome d oxidase. However, the SurB- phenotype is not simply attributable to the absence of cytochrome d oxidase. Thus, the surB gene product may have an additional role in the cell.

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