Transcriptional occlusion caused by overlapping promoters.
RpoS (σ(38)) is required for cell survival under stress conditions, but it can inhibit growth if produced inappropriately and, consequently, its production and activity are elaborately regulated. Crl, a transcriptional activator that does not bind DNA, enhances RpoS activity by stimulating the interaction between RpoS and the core polymerase. The crl gene has two overlapping promoters, a housekeeping, RpoD- (σ(70)) dependent promoter, and an RpoN (σ(54)) promoter that is strongly up-regulated under nitrogen limitation. However, transcription from the RpoN promoter prevents transcription from the RpoD promoter, and the RpoN-dependent transcript lacks a ribosome-binding site. Thus, activation of the RpoN promoter produces a long noncoding RNA that silences crl gene expression simply by being made. This elegant and economical mechanism, which allows a near-instantaneous reduction in Crl synthesis without the need for transacting regulatory factors, restrains the activity of RpoS to allow faster growth under nitrogen-limiting conditions.
Department of Molecular Biology, Princeton University, Princeton, NJ 08544.
M Ammar
MA
Zafar
Valerie J
VJ
Carabetta
Mark J
MJ
Mandel
Thomas J
TJ
Silhavy
D029968:Escherichia coli Proteins / Q000235:genetics; D005786:Gene Expression Regulation; D009584:Nitrogen / Q000378:metabolism; D011401:Promoter Regions, Genetic; D051877:RNA Polymerase Sigma 54 / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D014158:Transcription, Genetic
D029968:Escherichia coli Proteins; D012333:RNA, Messenger; C497751:rpoN protein, E coli; D051877:RNA Polymerase Sigma 54; D009584:Nitrogen
lncRNA; transcriptional repression