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Starvation survival in Listeria monocytogenes: characterization of the response and the role of known and novel components

Department of Molecular Biology and Biotechnology, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK¹

Author for correspondence: Simon J. Foster. Tel: +44 114 2224411. Fax: +44 114 2728697. e-mail: s.foster{at}sheffield.ac.uk

The starvation survival response (SSR) of Listeria monocytogenes EGD is induced under glucose- or multiple-nutrient-, but not amino-acid limitation. 0·01–0·2% of the population remain viable even after 20 d and the survivors show a reduced cell size and increased cross-protection to several environmental stresses. The development of the SSR may therefore be important in L. monocytogenes survival in the food environment. The initiation, but not the maintenance, of the SSR involves both protein and cell wall biosynthesis. It is also likely that nutrients released from dead cells are recycled to allow survival of the remaining population. To define the molecular mechanisms involved in the initiation, maintenance and release from the SSR the role of known, and novel, components was examined. The well-characterized regulators SigB and PrfA are both required for the full SSR and effect stress resistance during growth and starvation. A transposon mutagenesis screen identified two novel loci with roles in the SSR and stress resistance. Characterization of the transposon insertion sites revealed a putative homologue of the gene yulB from Bacillus subtilis and a gene of unknown function. The potential individual and combined roles of the SSR components are discussed.

Keywords: stress resistance, nutrient limitation, SigB, PrfA

Abbreviations: SSR, starvation survival response

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