CRL STIMULATES RPOS ACTIVITY DURING STATIONARY-PHASE

RpoS, an alternative primary sigma factor, has been shown to be regula ted at multiple levels, including transcription, translation and prote in stability. Here, we present evidence that suggests that RpoS is reg ulated at yet another level by the product of the crl gene. The crl ge ne was first thought to encode the major curlin subunit of curli (curl i are surface structures that are induced by growth into stationary ph ase under conditions of low osmolarity and low temperature). Later, it was determined that crl actually contributes in a positive fashion to stimulate transcription of csgBA, the true locus encoding for the maj or subunit of curli. RpoS is also required for normal stationary-phase induction of csgBA. We found that lesions in crl, like lesions in rpo S, cause increased transcription of ompF during stationary phase. Take n together, these observations prompted us to analyse the effects of c rl on an additional RpoS-regulated phenomenon. We found that a crl nul l allele influences expression of RpoS-regulated genes in a fashion si milar to an rpoS null allele. Genetic evidence suggests that crl and r poS function in a single pathway and that Crl functions upstream, or i n concert with, RpoS. Although the effects of Crl on RpoS-regulated ge nes is entirely dependent on the integrity of RpoS, the presence of a crl null allele does not decrease the level of RpoS protein. Thus, we propose that Crl stimulates the activity of the RpoS regulon by stimul ating RpoS activity during stationary phase.