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Mol Microbiol. 2016 Jan;99(2):254-73. doi: 10.1111/mmi.13230. Epub 2015 Oct 26.

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

Author information

1
Department of Microbiology, University of Illinois at Urbana-Champaign, 601 S. Goodwin Ave., Urbana, IL, 61801, USA.

Abstract

The Escherichia 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 ptsG and manXYZ mRNAs, which encode sugar transporters, and activates translation of yigL mRNA, encoding a sugar phosphatase. This study defines four new genes as direct targets of E. coli SgrS. These new targets, asd, adiY, folE and purR, 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 adiY and folE mRNAs suggest that SgrS pairing with these targets directly occludes ribosome binding and prevents translation initiation. SgrS binding within the purR coding sequence recruits the RNA chaperone Hfq to directly repress purR translation. Two separate SgrS binding sites were found on asd mRNA, and both are required for full translational repression. Ectopic overexpression of asd, adiY and folE 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.

PMID:
26411266
PMCID:
PMC4996119
DOI:
10.1111/mmi.13230
[Indexed for MEDLINE]
Free PMC Article

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