Role of Escherichia coli RpoS, LexA and H-NS global regulators in metabolism and survival under aerobic, phosphate-starvation conditions

It has been suggested that Escherichia coli can resist aerobic, glucose-sta rvation conditions by switching rapidly from an aerobic to a fermentative m etabolism, thereby preventing the production by the respiratory chain of re active oxygen species (ROS) that can damage cellular constituents. In contr ast, it has been reported that E. coli cannot resist aerobic, phosphate (Pi )starvation conditions, probably because of the maintenance of an aerobic m etabolism and the continuous production of ROS. This paper presents evidenc e that E. coli cells starved far Pi under aerobic conditions indeed maintai n an active aerobic metabolism for about 3 d, which allows the complete deg radation of exogenous nutrients such as arginine (metabolized probably to p utrescine via the SpeA-initiated pathway) and glucose (metabolized notably to acetate), but cell viability is not significantly affected because of th e protection afforded against ROS through the expression of the RpoS and Le xA regulons. The involvement of the LexA-controlled RuvAB and RecA proteins with the! RecG and RecBCD proteins in metabolism and cell viability implie s that RNA double-strand breaks (DSB), and thus hydroxyl radicals that norm ally generate this type of damage, are produced in P-i-starved cells. It is shown that induction of the LexA regulon, which helps protect Pi starved c ells, is totally prevented by introduction of a recB mutation, which indica tes that DSB are actually the main DNA lesion generated in P-i-starved cell s. The requirement of RpoS for survival of cells starved for Pi may thus be explained by the role played by various RpoS-controlled gene products such as KatE, KatG and Dps in the protection of DNA against ROS. In the same li ght, the degradation of arginine and threonine may be accounted for by the synthesis of polyamines (putrescine! and spermidine) that protect nucleic a cids from ROS. Resides LexA and RpoS, a third global regulator, the nucleoi d-associated protein H-NS, is also shown to play a key role in Pi-starved c ells. Through a modulation of the metabolism during Pi starvation, H-NS may perform two complementary tasks: it helps maintain a rapid metabolism of g lucose and arginine, probably by favouring tbe activity of aerobic enzymes such as the NAD-dependent pyruvate dehydrogenase complex, and it may enhanc e the cellular defences against ROS which are then produced by increasing R poS activity via the synthesis of acetate and presumably homoserine lactone .