ArticleJournal of bacteriology2013
Depletion of glycolytic intermediates plays a key role in glucose-phosphate stress in Escherichia coli.
Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 80 citations in OpenAlex.
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- Stoichiometric Modeling of Artificial String Chemistries Reveals Constraints on Metabolic Network Structure.Journal of molecular evolution · 2021Article
- A lysate proteome engineering strategy for enhancing cell-free metabolite production.Metabolic engineering communications · 2021Article
- Effects of individual base-pairs on in vivo target search and destruction kinetics of bacterial small RNA.Nature communications · 2021Article
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- Yeast cell wall mannan rich fraction modulates bacterial cellular respiration potentiating antibiotic efficacy.Scientific reports · 2020Article
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- Stratified reconstruction of ancestral Escherichia coli diversification.BMC genomics · 2019Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
In bacteria like Escherichia coli, the accumulation of glucose-6-phosphate (G6P) or its analogs such as α-methyl glucoside-6-phosphate (αMG6P) results in stress that appears in the form of growth inhibition. The small RNA SgrS is an essential part of the response that helps E. coli combat glucose-phosphate stress; the growth of sgrS mutants during stress caused by αMG is significantly impaired. The cause of this stress is not currently known but may be due to either toxicity of accumulated sugar-phosphates or to depletion of metabolic intermediates. Here, we present evidence that glucose-phosphate stress results from depletion of glycolytic intermediates. Addition of glycolytic compounds like G6P and fructose-6-phosphate rescues the αMG growth defect of an sgrS mutant. These intermediates also markedly decrease induction of the stress response in both wild-type and sgrS strains grown with αMG, implying that cells grown with these intermediates experience less stress. Moreover, αMG transport assays confirm that G6P relieves stress even when αMG is taken up by the cell, strongly suggesting that accumulated αMG6P per se does not cause stress. We also report that addition of pyruvate during stress has a novel lethal effect on the sgrS mutant, resulting in cell lysis. The phosphoenolpyruvate (PEP) synthetase PpsA, which converts pyruvate to PEP, can confer resistance to pyruvate-induced lysis when ppsA is ectopically expressed in the sgrS mutant. Taken as a whole, these results provide the strongest evidence thus far that depletion of glycolytic intermediates is at the metabolic root of glucose-phosphate stress.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.