Single deletion of fRMsr has complete growth inhibition on methionine-R-sulfoxide medium and double fRMsr/MXR1 deletion completely blocks the growth on both methionine-R-sulfoxide and methionine-S-sulfoxide medium. Double fRMsr/MXR2 deletion has no effect on growth on methionine-S-sulfoxide medium. Single mutant or any of the double mutants show no growth defects in methionine medium, even the triple fRMsr/MXR1/MXR2 deletion mutant is viable and grows similarly to wild-type. Single deletion of fRMsr has an increased sensitivity to oxidative stress and a decreased life span of 18% compared to wild-type. Double fRMsr/MXR1 and fRMsr/MXR2 deletion mutants as well as triple fRMsr/MXR1/MXR2 deletion mutant show 20% reduction in life span compared with wild-type cells.
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Single deletion of fRMsr has complete growth inhibition on methionine-R-sulfoxide medium and double fRMsr/MXR1 deletion completely blocks the growth on both methionine-R-sulfoxide and methionine-S-sulfoxide medium. Double fRMsr/MXR2 deletion has no effect on growth on methionine-S-sulfoxide medium. Single mutant or any of the double mutants show no growth defects in methionine medium, even the triple fRMsr/MXR1/MXR2 deletion mutant is viable and grows similarly to wild-type. Single deletion of fRMsr has an increased sensitivity to oxidative stress and a decreased life span of 18% compared to wild-type. Double fRMsr/MXR1 and fRMsr/MXR2 deletion mutants as well as triple fRMsr/MXR1/MXR2 deletion mutant show 20% reduction in life span compared with wild-type cells.
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