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Curr Opin Microbiol. 2007 Apr;10(2):146-51. Epub 2007 Mar 23.

Physiological consequences of small RNA-mediated regulation of glucose-phosphate stress.

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  • 1Department of Microbiology, University of Illinois at Urbana-Champaign B213, Chemical and Life Sciences Laboratories (CLSL), MC-110 Urbana, IL 61801, USA.


Accumulation of non-metabolizable glucose-phosphate in Escherichia coli is growth inhibitory and induces a specific stress response. This is sensed and coordinated by a transcription factor SgrR that in turn activates expression of the primary effector of the stress response, a small regulatory RNA, SgrS. This RNA negatively regulates the translation and stability of the ptsG mRNA, which encodes the major glucose transporter of E. coli. The effect of SgrS on ptsG mRNA occurs through a base-pairing mechanism facilitated by the RNA chaperone Hfq. Other host factors required for the regulation by SgrS include the endonuclease RNase E and components of the RNA degradosome, particularly enolase, a glycolytic enzyme whose role in RNA degradation is currently not understood. There are many unanswered questions regarding the physiology of glucose-phosphate stress, including the cellular signals and targets involved. However, it is clear that the small RNA SgrS is required for adaptation to stress. The current model is that SgrS promotes recovery by stopping the synthesis of glucose transport proteins, which in turn limits the accumulation of toxic sugar-phosphates.

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