A mutation in the Escherichia coli gene encoding the stationary phase-
inducible sigma factor (sigma(S), RpoS) not only abolishes transcripti
on of some genes in stationary phase, but also causes superinduction o
f other stationary phase-induced genes. We have examined this phenomen
on of repression by sigma(S) using as a model system the divergently t
ranscribed stationary phase-inducible genes, uspA and uspB. uspA is tr
anscribed by sigma(70)-programmed RNA polymerase and is superinduced i
n an rpoS mutant, while uspB induction is sigma(S) dependent. The data
suggest that the superinduction of uspA is caused by an increased amo
unt of sigma(70) bound to RNA polymerase in the absence of the competi
ng sigma(S). Increasing the ability of sigma(70) to compete against si
gma(S) by overproducing sigma(70) mimics the effect of an rpoS mutatio
n by causing superinduction of sigma(70)-dependent stationary phase-in
ducible genes (uspA and fadD), silencing of sigma(S)-dependent genes (
uspB, bolAp1 and fadL) and inhibiting the development of os-dependent
phenotypes, such as hydrogen peroxide resistance in stationary phase.
In addition, overproduction of sigma(S) markedly reduced stationary ph
ase expression of a sigma(70)-dependent promoter, Thus, we conclude th
at sigma factors compete for a limiting amount of RNA polymerase durin
g stationary phase, The implications of this competition in the passiv
e control of promoter activity is discussed.