Abstract
Lesions to DNA compromise chromosome integrity, posing a direct threat to cell survival. The bacterial SOS response is a widespread transcriptional regulatory mechanism to address DNA damage. This response is coordinated by the LexA transcriptional repressor, which controls genes involved in DNA repair, mutagenesis and cell-cycle control. To date, the SOS response has been characterized in most major bacterial groups, with the notable exception of the Bacteroidetes. No LexA homologs had been identified in this large, diverse and ecologically important phylum, suggesting that it lacked an inducible mechanism to address DNA damage. Here, we report the identification of a novel family of transcriptional repressors in the Bacteroidetes that orchestrate a canonical response to DNA damage in this phylum. These proteins belong to the S24 peptidase family, but are structurally different from LexA. Their N-terminal domain is most closely related to CI-type bacteriophage repressors, suggesting that they may have originated from phage lytic phase repressors. Given their role as SOS regulators, however, we propose to designate them as non-canonical LexA proteins. The identification of a new class of repressors orchestrating the SOS response illuminates long-standing questions regarding the origin and plasticity of this transcriptional network.
Highlights
Many environmental insults and endogenous processes can cause DNA lesions that pose a direct threat to cell survival
Comparative analyses have established that error-prone polymerases constitute the conserved core SOS response across bacteria, presumably due to the need to mitigate the high mutagenic load of unregulated error-prone polymerases [1,10,15]
The SOS regulation of a putative uracilDNA glycosylase-based DNA base excision repair system has been reported in the Verrucomicrobia and the Alphaproteobacteria [7,65]
Summary
Many environmental insults and endogenous processes can cause DNA lesions that pose a direct threat to cell survival. First described in Escherichia coli, the SOS response involves the coordinated expression of over 40 genes encoding primarily DNA repair and recombination enzymes, translesion synthesis polymerases and cell division inhibitors [3,4]. This process is governed by the LexA repressor. This protein forms dimers that bind to operator sites in the promoter region of regulated operons by targeting a highly specific palindromic motif (CTGT-N8-ACAG in E. coli) [3]. Upon self-cleavage, the LexA dimer detaches from its operator sites, derepressing regulated operons and inducing the SOS response [4]
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