To be or not to be: the ultimate decision of the growth-arrested bacterial cell

The evolutionary survival of prokaryotes has depended not only on their performance during conditions that allow rapid growth, but also on their ability to adjust their internal affairs to enhance survival during prolonged periods of growth arrest. The small size of prokaryotes limits their ability to control their environment, and instead, their ability to cope with environmental challenges must rely on rapid and efficient control of gene expression. The majority of genes responding to a specific environmental condition causing growth arrest are, in general, uniquely induced by one specific stimulus. However, many genes, operons and regulons do not exclusively respond to one particular stress condition, and some regulons appear to be related in the sense that they share member genes. Furthermore, growth-arrest conditions activate several seemingly unlinked regulatory networks and several genes/proteins seem to respond to growth arrest in general. These proteins are interesting because we know very little about why growth-arrested, stationary phase cells ultimately die, and functional analysis of such general responders to growth arrest may help us to understand the genetic/biochemical basis for the bacterial defence against ageing processes. In this paper I review recent findings suggesting that several general responders to stasis form an integral part of a defence system aimed at avoiding the damaging effects of endogenously generated oxygen radicals. In addition, the curious finding that some proteins of a regulon are involved in enhancing the life-span of the growth-arrested cell while other members of the same regulon are devoted to killing it will be discussed.