| Literature DB >> 33605213 |
Camille Henry1,2, Laurent Loiseau1, Alexandra Vergnes1, Didier Vertommen3, Angela Mérida-Floriano4, Sindhu Chitteni-Pattu2, Elizabeth A Wood2, Josep Casadesús4, Michael M Cox2, Frédéric Barras1,5,6, Benjamin Ezraty1.
Abstract
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.Entities:
Keywords: E. coli; RecA; infectious disease; methionine sulfoxide; microbiology; oxidative damage; redox
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Year: 2021 PMID: 33605213 PMCID: PMC7943192 DOI: 10.7554/eLife.63747
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.140