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  • Title: ImuA Facilitates SOS Mutagenesis by Inhibiting RecA-Mediated Activity in Myxococcus xanthus.
    Author: Sheng D, Wang Y, Jiang Z, Liu D, Li Y.
    Journal: Appl Environ Microbiol; 2021 Aug 26; 87(18):e0091921. PubMed ID: 34190612.
    Abstract:
    Bacteria have two pathways to restart stalled replication forks caused by environmental stresses, error-prone translesion DNA synthesis (TLS) catalyzed by TLS polymerase and error-free template switching catalyzed by RecA, and their competition on the arrested fork affects bacterial SOS mutagenesis. DnaE2 is an error-prone TLS polymerase, and its functions require ImuA and ImuB. Here, we investigated the transcription of imuA, imuB, and dnaE2 in UV-C-irradiated Myxococcus xanthus and found that the induction of imuA occurred significantly earlier than that of the other two genes. Mutant analysis showed that unlike that of imuB or dnaE2, the deletion of imuA significantly delayed bacterial regrowth and slightly reduced the bacterial mutation frequency and UV resistance. Transcriptomic analysis revealed that the absence of ImuA released the expression of some known SOS genes, including recA1, recA2, imuB, and dnaE2. Yeast two-hybrid and pulldown analyses proved that ImuA interacts physically with RecA1 besides ImuB. Protein activity analysis indicated that ImuA had no DNA-binding activity but inhibited the DNA-binding and recombinase activity of RecA1. These findings indicate the new role of ImuA in SOS mutagenesis; that is, ImuA inhibits the recombinase activity of RecA1, thereby facilitating SOS mutagenesis in M. xanthus. IMPORTANCE DnaE2 is responsible for bacterial SOS mutagenesis in nearly one-third of sequenced bacterial strains. However, its mechanism, especially the function of one of its accessory proteins, ImuA, is still unclear. Here, we report that M. xanthus ImuA could affect SOS mutagenesis by inhibiting the recombinase activity of RecA1, which helps to explain the mechanism of DnaE2-dependent TLS and the selection of the two restart pathways to repair the stalled replication fork.
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