BB0761, a MepM homolog, contributes to Borrelia burgdorferi cell division and mammalian infectivity.

BB0761, a MepM homolog, contributes to Borrelia burgdorferi cell division and mammalian infectivity.
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MEPM同源物BB0761为Borrelia Burgdorferi细胞分裂和哺乳动物感染力做出了贡献。

DOI:
10.1111/mmi.14916
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发表时间:
2022-06
影响因子:
3.6
通讯作者:
Ouyang, Zhiming
Ouyang, Zhiming
中科院分区:
生物学2区
文献类型:
--
作者:
Thompson, Christina;George, Sierra;White, Maria L.;Eswara, Prahathees J.;Ouyang, Zhiming

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M23家族内肽酶在多种细菌的细胞分裂和分离中发挥重要作用。最近的研究表明,这些蛋白质也有助于细菌的毒力。然而,M23肽酶在致病性螺旋体中的生物学功能仍然未被探索。在这里,我们描述了伯氏疏螺旋体,细菌病原体引起莱姆病,需要一个假定的M23家族同系物,BB0761,螺旋体形态和细胞分裂。事实上,bb0761的失活导致异常的丝状表型以及B的损伤。Burgdorferi体外生长。这些表型不仅与B互补。burgdorferi bb0761的mepM基因,也与E.杆菌此外,bb0761突变体在莱姆疏螺旋体病的鼠模型中表现出完全丧失感染性。突变体对渗透胁迫和氧化胁迫的抗性显著降低。我们的综合结果表明,BB 0761有助于B。burgdorferi细胞分裂和毒性。
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.
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