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pubmed:abstractText |
RpoS, an alternative primary sigma factor, has been shown to be regulated at multiple levels, including transcription, translation and protein stability. Here, we present evidence that suggests that RpoS is regulated at yet another level by the product of the crl gene. The crl gene was first thought to encode the major curlin subunit of curli (curli are surface structures that are induced by growth into stationary phase 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 major subunit of curli. RpoS is also required for normal stationary-phase induction of csgBA. We found that lesions in crl, like lesions in rpoS, cause increased transcription of ompF during stationary phase. Taken together, these observations prompted us to analyse the effects of crl on an additional RpoS-regulated phenomenon. We found that a crl null allele influences expression of RpoS-regulated genes in a fashion similar to an rpoS null allele. Genetic evidence suggests that crl and rpoS function in a single pathway and that Crl functions upstream, or in concert with, RpoS. Although the effects of Crl on RpoS-regulated genes 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 stimulating RpoS activity during stationary phase.
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