dsrA encodes a small, untranslated RNA. When over-expressed, DsrA antagonizes the H-NS-mediated silencing of numerous promoters. Cells devoid of DsrA grow normally and show little change in the expression of a number of H-NS-silenced genes. Expression of a transcriptional fusion of lacZ to dsrB, the gene next to dsrA, is significantly lower in cells carrying mutations in dsrA. All expression of beta-galactosidase from the dsrB::lacZ fusion is also dependent on the stationary phase sigma factor, RpoS. DsrA RNA was found to regulate dsrB::lacZ indirectly, by modulating RpoS synthesis. Levels of RpoS protein are substantially lower in a dsrA mutant, both in stationary and exponential phase cells. Mutations in dsrA decrease the expression of an RpoS::LacZ translational fusion, but not a transcriptional fusion, suggesting that DsrA is acting after transcription initiation. While RpoS expression is very low in exponential phase at temperatures of 30 degrees C and above, at 20 degrees C there is substantial synthesis of RpoS during exponential growth, all dependent on DsrA RNA. dsrA expression is also increased at low temperatures. These results suggest a new role for RpoS during exponential growth at low temperatures, mediated by DsrA.