Abstract
The flavin mononucleotide (FMN) riboswitch is structured noncoding RNA domains that control gene expression by selectively binding FMN or sensing surrounding changes without protein factors, which are involved in the biosynthesis and transport of riboflavin and related compounds. We constructed the deletion mutant of FMN riboswitch to investigate its possible role in response to H2O2 stress in Deinococcus radiodurans. The results showed that the deletion of FMN riboswitch resulted in an obvious growth delay in D. radiodurans. Compared with the survival rate of 56% of D. radiodurans, only 40% of the mutant survived after treated with 50mM of H2O2, indicating that deletion of FMN riboswitch obviously increased the susceptibility to H2O2. Compared with the wild type R1 strain of D. radiodurans, FMN riboswitch knockout cells accumulated a higher level of intracellular reactive oxygen species (ROS) while their total catalase activity reduced significantly. Results from quantitative real-time PCR analysis implies structural alterations of in response to H2O2 challenge. Our data suggest a critical role of FMN riboswitch in the oxidation tolerance system of D. radiodurans.
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