Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS.
Previous work showed that about 85% of stress-induced mutations associated with DNA double-strand break repair in carbon-starved Escherichia coli result from error-prone DNA polymerase IV (Pol IV) (DinB) and that the mutagenesis is controlled by the RpoS stress response, which upregulates dinB. We report that the remaining mutagenesis requires high-fidelity Pol II, and that this component also requires RpoS. The results identify a second DNA polymerase contributing to stress-induced mutagenesis and show that RpoS promotes mutagenesis by more than the simple upregulation of dinB.
Frisch
Ryan L
RL
Department of Molecular and Human Genetics, Baylor College of Medicine,Baylor College of Medicine, Houston, Texas 77030-3411, USA.
Su
Yang
Y
Thornton
P C
PC
Gibson
Janet L
JL
Rosenberg
Susan M
SM
Hastings
P J
PJ
D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D004257:DNA Polymerase II / Q000235:genetics / Q000378:metabolism*; D019951:DNA Polymerase beta / Q000235:genetics / Q000378:metabolism*; D004260:DNA Repair / Q000235:genetics; D004926:Escherichia coli / Q000201:enzymology* / Q000235:genetics*; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D016296:Mutagenesis; D009154:Mutation / Q000235:genetics; D012808:Sigma Factor / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*
D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; D012808:Sigma Factor; C069567:sigma factor KatF protein, Bacteria; D004257:DNA Polymerase II; D019951:DNA Polymerase beta