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In bacteria, cytoplasmic levels of the effector nucleotide ppGpp are regulated in response to changes in growth conditions. This study describes the involvement of SpoT-mediated ppGpp accumulation in the survival of lightexposed bacteria during fatty acid starvation. In contrast to isogenic wild-type strains and relA mutants, the ' Vibrio angustum ' S14 spoT and Escherichia coli relA spoT mutants displayed significant losses in viability in response to cerulenin-induced fatty acid starvation under cool-white fluorescent light. However, when starvation experiments were performed in complete darkness, or under light filtered through a UV-resistant perspex sheet, only a minor decline in viability was observed for the wild-type and mutant strains. This finding indicated that the lethal effect was mediated by weak UV emission. In contrast to the E. coli relA spoT mutant, which lacks ppGpp, the ' V. angustum ' S14 spoT mutant exhibited higher ppGpp levels and lower RNA synthesis rates during fatty acid starvation, features that might be correlated with its lethality. In agreement with this finding, fatty acid starvation lethality also occurred upon induction of ppGpp overaccumulation in E. coli. These data suggest that the precise regulation of ppGpp levels in the stressed cell is crucial, and that both the absence and the overaccumulation of ppGpp impair fatty acid starvation survival of light-exposed cells. Moreover, the UV-induced lethal effect during fatty acid starvation was also observed for E. coli strains mutated in rpoS and dps, which, in the wild-type, are regulated directly or indirectly by ppGpp, respectively. The restoration of viability of fatty-acidstarved spoT mutant cells through the addition of exogenous catalase suggested that the observed light-dependent lethal effect was, at least in part, caused by UV-imposed oxidative stress. Based on these results, it is proposed that fatty acid starvation adaptation of light-exposed bacterial cells depends on the development of resistance to UV-induced oxidative stress. This stress resistance was found to require appropriate ppGpp levels, ppGpp-induced RpoS expression and, hence, upregulation of RpoS-regulated stress-defending genes, such as dps.

It now seems clear that starvation adaptation is important for cells to initiate long-term survival under conditions of not only nutrient depletion but to develop resistance to other stresses, most notably oxidative stress. Clearly, oxidative stress is a condition likely to be perceived by many bacteria, for example, in the form of reactive oxygen species derived from metabolic processes or from near-UV exposure. We have found evidence for a large degree of overlap in the cell's use of global regulators to deal with both starvation and oxidative stress. Both SpoT and AI-2 signalling pathways are important regulators of starvation and stress adaptation as well as the alternative sigma factor, RpoE. We also present evidence that suggests that AI-2 signalling can mediate starvation adaptation at the molecular level by increasing the stability of the mRNAs so that cells are prepared for rapid response to nutrient addition. Moreover, such extracellular signals mediate intraspecies communication to enable enhanced survival and stress resistance of neighbouring bacterial cells. It is likely that bacteria rely on a suite of effects between cells and on transcription, translation and post-translationalprocesses, mediated by global regulators and signalling molecules, to meet their needs for growth and survival.