A mutation in the Escherichia coli gene encoding the stationary phase-inducible sigma factor (sigmaS, RpoS) not only abolishes transcription of some genes in stationary phase, but also causes superinduction of other stationary phase-induced genes. We have examined this phenomenon of repression by sigmaS using as a model system the divergently transcribed stationary phase-inducible genes, uspA and uspB. uspA is transcribed by sigma70-programmed RNA polymerase and is superinduced in an rpoS mutant, while uspB induction is sigmaS dependent. The data suggest that the superinduction of uspA is caused by an increased amount of sigma70 bound to RNA polymerase in the absence of the competing sigmaS. Increasing the ability of sigma70 to compete against sigmaS by overproducing sigma70 mimics the effect of an rpoS mutation by causing superinduction of sigma70-dependent stationary phase-inducible genes (uspA and fadD), silencing of sigmaS-dependent genes (uspB, bolAp1 and fadL) and inhibiting the development of sigmaS-dependent phenotypes, such as hydrogen peroxide resistance in stationary phase. In addition, overproduction of sigmaS markedly reduced stationary phase expression of a sigma70-dependent promoter. Thus, we conclude that sigma factors compete for a limiting amount of RNA polymerase during stationary phase. The implications of this competition in the passive control of promoter activity is discussed.