Recovery of respiration following the SOS response of Escherichia coli requires RecA-mediated induction of 2-keto-4-hydroxyglutarate aldolase

Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11806-9. doi: 10.1073/pnas.92.25.11806.

Abstract

Agents that damage DNA in Escherichia coli or interfere with its replication induce DNA repair and mutagenesis via the SOS response. This well-known activity is regulated by the RecA protein and the LexA repressor. Following repair or bypass of the DNA lesion, the cell returns to its resting state by a largely unknown process. We found that 2-keto-4-hydroxyglutarate aldolase (4-hydroxy-2-oxoglutarate aldolase; EC 4.1.3.16) is necessary for the recovery of respiration and that it is regulated by the SOS response. This protein was induced by DNA-damaging agents. Induction required RecA activation. When the LexA regulon was repressed, activation of RecA was not sufficient for induction, indicating the requirement for an additional protein under LexA control. Finally, a mutant in the corresponding hga gene was UV sensitive. 2-Keto-4-hydroxyglutarate aldolase also plays a role in respiratory metabolic pathways, which suggests a mechanism for respiration resumption during the termination of the SOS response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Dose-Response Relationship, Radiation
  • Enzyme Induction
  • Escherichia coli / enzymology
  • Escherichia coli / physiology*
  • Escherichia coli / radiation effects
  • Gene Expression Regulation, Bacterial
  • Kanamycin Resistance
  • Models, Biological
  • Molecular Sequence Data
  • Oxo-Acid-Lyases / biosynthesis*
  • Oxygen Consumption*
  • Rec A Recombinases / metabolism*
  • SOS Response, Genetics*
  • Ultraviolet Rays / adverse effects

Substances

  • Rec A Recombinases
  • Oxo-Acid-Lyases
  • 4-hydroxy-2-oxoglutarate aldolase