Project description:DNA damage induces the mutations that drive bacterial adaption, evolution, and antibiotic escape. Both mutagenic and non-mutagenic DNA damage repair is coordinated by the SOS response, but despite extensive work, the functions of some SOS-induced genes remain obscure. Here, we clarify the function of Escherichia coli SbmC (GyrI). Despite its proposed function as a gyrase inhibitor, cells either lacking or overexpressing SbmC instead exhibit phenotypes consistent with a role in limiting DNA damage and cellular variation. Importantly, SbmC levels inversely correlate with E. coli mutation rate. Excess SbmC limits mutation whereas loss of SbmC increases mutation, possibly because ∆sbmC cells variably induce the SOS response, including mutagenic DNA Pol V. We additionally show that SbmC is dispensable for survival in the presence of double-strand break inducing drugs but is required to limit their mutational effects. Finally, evolutionary analysis indicates that bacterial SbmC homologs maintain their small molecule-binding domain but not the gyrase interacting residues identified in E. coli. Together, our findings suggest that SbmC-like proteins may bind to a yet-unknown cofactor to limit DNA damage and organismal evolution.

2026-03-11 | GSE324174 | GEO

Nitrogen Starvation Induces Persister Cell Formation in Escherichia coli.

Project description: Not available

| S-EPMC6349093 | biostudies-literature

Proteomic adaptations to starvation prepare Escherichia coli for disinfection tolerance.

Project description: Not available

| S-EPMC4351261 | biostudies-literature

Transcriptome analysis of Escherichia coli during dGTP Starvation

Project description:Our laboratory has recently discovered that E. coli cells starved for the DNA precursor dGTP are killed efficiently (dGTP starvation) in a manner similar to that described for Thymineless Death (TLD). Conditions for specific dGTP starvation can be achieved by depriving an E. coli optA1 gpt strain of the purine nucleotide precursor hypoxanthine (Hx). To gain insight into the mechanisms underlying dGTP starvation, we conducted genome-wide gene expression analyses on actively growing optA1 gpt strains subjected to hypoxanthine deprivation for increasing periods of time. The data show that, upon Hx withdrawal, the optA1 gpt strain displays a diminished ability to de-repress the de novo purine biosynthesis genes, and this is likely due to internal guanine accumulation. The impairment to fully induce the purR regulon may be a contributing factor to the lethality of dGTP starvation. At later time points, and coinciding with cell lethality, strong induction of the SOS is observed, supporting the concept of replication stress as a final cause of death. No evidence was observed for the participation of other stress responses, including the rpoS-mediated global stress response in the starved cells, and reinforcing the lack of feedback of replication stress into the global metabolism of the cell. The genome-wide expression data also provide direct evidence for increased genome complexity during dGTP starvation, as a markedly increased gradient is observed for expression of genes located nearby the replication origin relative to those located towards the replication terminus.

2016-04-06 | GSE80002 | GEO

Growth and Maintenance of Escherichia coli Laboratory Strains.

Project description: Not available

| S-EPMC8006063 | biostudies-literature