@article{a3f99610a7fc49bd9d8e341b6c1ec0c2,
title = "BB0761, a MepM homolog, contributes to Borrelia burgdorferi cell division and mammalian infectivity",
abstract = "M23 family endopeptidases play important roles in cell division and separation in a wide variety of bacteria. Recent studies have suggested that these proteins also contribute to bacterial virulence. However, the biological function of M23 peptidases in pathogenic spirochetes remains unexplored. Here, we describe Borrelia burgdorferi, the bacterial pathogen causing Lyme disease, requires a putative M23 family homolog, BB0761, for spirochete morphology and cell division. Indeed, the inactivation of bb0761 led to an aberrant filamentous phenotype as well as the impairment of B. burgdorferi growth in vitro. These phenotypes were complemented not only with B. burgdorferi bb0761, but also with the mepM gene from E. coli. Moreover, the bb0761 mutant showed a complete loss of infectivity in a murine model of Lyme borreliosis. Resistance of the mutant to osmotic and oxidative stresses was markedly reduced. Our combined results indicate that BB0761 contributes to B. burgdorferi cell division and virulence.",
keywords = "Borrelia burgdorferi, gene regulation, lyme disease, pathogenesis, protease, virulence",
author = "Christina Thompson and Sierra George and White, {Maria L.} and Eswara, {Prahathees J.} and Zhiming Ouyang",
note = "Funding Information: We thank Dr. Thomas Bernhardt, Harvard Medical School, Harvard University, for providing E. coli K12 strain TB28 and the mepM deletion mutant TD10. We also thank Dr. Chang-Ro Lee, Department of Biological Sciences and Bioinformatics, Myongji University for providing E. coli K12 strain MG1655 and the mepM mutant. This work was supported by funding from the National Institutes of Health AI146909 (ZO), AI159061 (ZO), AI152983 (ZO), and R35GM133617 (PJE). The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. Funding Information: We thank Dr. Thomas Bernhardt, Harvard Medical School, Harvard University, for providing K12 strain TB28 and the deletion mutant TD10. We also thank Dr. Chang‐Ro Lee, Department of Biological Sciences and Bioinformatics, Myongji University for providing K12 strain MG1655 and the mutant. This work was supported by funding from the National Institutes of Health AI146909 (ZO), AI159061 (ZO), AI152983 (ZO), and R35GM133617 (PJE). The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. E. coli mepM E. coli mepM Publisher Copyright: {\textcopyright} 2022 John Wiley & Sons Ltd.",
year = "2022",
month = jun,
doi = "10.1111/mmi.14916",
language = "English (US)",
volume = "117",
pages = "1405--1418",
journal = "Molecular Microbiology",
issn = "0950-382X",
publisher = "Wiley-Blackwell",
number = "6",
}