Non-canonical LexA proteins regulate the SOS response in the Bacteroidetes

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https://academic.oup.com/nar/article/49/19/11050/6382392

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https://doi.org/10.1093/nar/gkab773
 http://hdl.handle.net/11603/23216

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UMBC Chemistry & Biochemistry Department
UMBC Biological Sciences Department
UMBC Computer Science and Electrical Engineering Department
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https://orcid.org/0000-0003-0660-7359
 https://orcid.org/0000-0002-9332-8683
 https://orcid.org/0000-0002-7280-7191

Date

2021-10-06

Type of Work

journal articles
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Citation of Original Publication

Sánchez-Osuna, Miquel et al.; Non-canonical LexA proteins regulate the SOS response in the Bacteroidetes; Nucleic Acids Research, Volume 49, Issue 19, Pages 11050–11066, 6 October, 2021; https://doi.org/10.1093/nar/gkab773

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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.