作者: Viviane Grazielle-Silva , Tehseen Fatima Zeb , Richard Burchmore , Carlos Renato Machado , Richard McCulloch
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摘要: MSH2, associated with MSH3 or MSH6, is a central component of the eukaryotic DNA Mismatch Repair (MMR) pathway responsible for recognition and correction base mismatches that occur during replication recombination. Previous studies have shown MSH2 plays an additional repair role in response to oxidative damage Trypanosoma cruzi brucei. By performing co-immunoprecipitation followed by mass spectrometry parasites expressing tagged proteins, we confirmed parasites’ forms complexes MSH6. To investigate involvement these two other MMR components stress response, generated knockout mutants MSH6 T. brucei bloodstream epimastigotes. Differently from phenotype observed epimastigotes, loss one alleles msh6 resulted increased susceptibility H2O2 exposure, besides impaired MMR. In contrast, msh3 null displayed tolerance MNNG treatment, indicating affected, but no difference treatment when compared wild type cells. Taken together, our results suggest that, while are involved addition their as MMR, deals operates differently