The evolutionary survival of prokaryotes has depended not only on thei
r performance during conditions that allow rapid growth, but also on t
heir ability to adjust their internal affairs to enhance survival duri
ng prolonged periods of growth arrest. The small size of prokaryotes l
imits their ability to control their environment, and instead, their a
bility to cope with environmental challenges must rely on rapid and ef
ficient control of gene expression. The majority of genes responding t
o a specific environmental condition causing growth arrest are, in gen
eral, uniquely induced by one specific stimulus. However, many genes,
operons and regulons do not exclusively respond to one particular stre
ss condition, and some regulons appear to be related in the sense that
they share member genes. Furthermore, growth-arrest conditions activa
te several seemingly unlinked regulatory networks and several genes/pr
oteins seem to respond to growth arrest in general. These proteins are
interesting because we know very little about why growth-arrested, st
ationary phase cells ultimately die, and functional analysis of such g
eneral responders to growth arrest may help us to understand the genet
ic/biochemical basis for the bacterial defence against ageing processe
s. In this paper I review recent findings suggesting that several gene
ral responders to stasis form an integral part of a defence system aim
ed at avoiding the damaging effects of endogenously generated oxygen r
adicals. In addition, the curious finding that some proteins of a regu
lon are involved in enhancing the life-span of the growth-arrested cel
l while other members of the same regulon are devoted to killing it wi
ll be discussed. (C) 1998 Federation of European Microbiological Socie
ties. Published by Elsevier Science B.V.