Diverse mechanisms of post‐transcriptional repression by the small RNA regulator of glucose‐phosphate stress

Summary The E scherichia coli small RNA SgrS controls a metabolic stress response that occurs upon accumulation of certain glycolytic intermediates. SgrS base pairs with and represses translation of pts G and man XYZ m RNA s, which encode sugar transporters, and activates translation of yig L m RNA , encoding a sugar phosphatase. This study defines four new genes as direct targets of E . coli   SgrS . These new targets, asd , adi Y , fol E and pur R , encode transcription factors or enzymes of diverse metabolic pathways, including aspartate semialdehyde dehydrogenase, arginine decarboxylase gene activator, GTP cyclohydrolase I and a repressor of purine biosynthesis, respectively. SgrS represses translation of each of the four target mRNAs via distinct mechanisms. SgrS binding sites overlapping the Shine–Dalgarno sequences of adi Y and fol E m RNA s suggest that SgrS pairing with these targets directly occludes ribosome binding and prevents translation initiation. SgrS binding within the pur R coding sequence recruits the RNA chaperone H fq to directly repress pur R translation. Two separate SgrS binding sites were found on asd m RNA , and both are required for full translational repression. Ectopic overexpression of asd , adi Y and fol E is specifically detrimental to cells experiencing glucose‐phosphate stress, suggesting that SgrS ‐dependent repression of the metabolic functions encoded by these targets promotes recovery from glucose‐phosphate stress.