All organisms experience environmental stressors such as fluctuations in nutrient availability. Glucose-phosphate stress is a growth inhibition in bacteria like Escherichia coli that results from blockages in the glycolytic pathway and related nutrient depletion. The transcription factor SgrR and the small RNA SgrS are essential to the recovery from this stress, in part by blocking transport of sugar-phosphates into the cell. We previously showed that the transcription factor DksA and the nucleotide alarmone ppGpp, regulators of the stringent response to nutrient starvation, are also needed to help E. coli recover from glucose-phosphate stress, in part by increasing expression of sgrR and sgrS. Here, we examine the effect of SgrR and SgrS on the recovery from stringent starvation. sgrR and sgrS gene deletion mutants were screened for changes in growth compared to wild-type E. coli under a variety of stringent conditions, including amino acid, carbon, iron, and phosphate starvation. Of all the conditions tested, the sgrR and sgrS mutants exhibited growth defects only under conditions of stringent carbon starvation. This carbon starvation-specific growth defect is consistent with the role of SgrR and SgrS in the recovery from glucose-phosphate stress, which is associated with the blocks in carbon metabolism. Because the stringent regulator ppGpp is a nucleotide derivative synthesized under conditions of stress, current research is focused on the role of genes related to the regulation and de novo synthesis of nucleotides during glucose-phosphate stress.
