Redox controls RecA protein activity via reversible oxidation of its methionine residues.
Camille HenryLaurent LoiseauAlexandra VergnesDidier VertommenAngela Mérida-FlorianoSindhu Chitteni-PattuElizabeth A WoodJosep CasadesúsMichael M CoxFrédéric BarrasBenjamin EzratyPublished in: eLife (2021)
Reactive oxygen species (ROS) cause damage to DNA and proteins. Here, we report that the RecA recombinase is itself oxidized by ROS. Genetic and biochemical analyses revealed that oxidation of RecA altered its DNA repair and DNA recombination activities. Mass spectrometry analysis showed that exposure to ROS converted four out of nine Met residues of RecA to methionine sulfoxide. Mimicking oxidation of Met35 by changing it for Gln caused complete loss of function, whereas mimicking oxidation of Met164 resulted in constitutive SOS activation and loss of recombination activity. Yet, all ROS-induced alterations of RecA activity were suppressed by methionine sulfoxide reductases MsrA and MsrB. These findings indicate that under oxidative stress MsrA/B is needed for RecA homeostasis control. The implication is that, besides damaging DNA structure directly, ROS prevent repair of DNA damage by hampering RecA activity.
Keyphrases
- dna damage
- dna repair
- oxidative stress
- reactive oxygen species
- diabetic rats
- cell death
- circulating tumor
- hydrogen peroxide
- mass spectrometry
- cell free
- tyrosine kinase
- amino acid
- electron transfer
- ischemia reperfusion injury
- genome wide
- induced apoptosis
- gene expression
- nucleic acid
- nitric oxide
- small molecule
- tandem mass spectrometry
- liquid chromatography
- simultaneous determination
- circulating tumor cells