Increasing RpoS expression causes cell death in Borrelia burgdorferi.

Increasing RpoS expression causes cell death in Borrelia burgdorferi.
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DOI:
10.1371/journal.pone.0083276
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Liang FT
Liang FT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Chen L;Xu Q;Tu J;Ge Y;Liu J;Liang FT

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RPOS是伯氏疏螺旋体的两个可选σ因子之一,受多个调控因子的严格调控,进而决定许多关键毒力因子的表达。在这里,我们表明,增加rpos的表达导致细胞死亡。增加rpos表达的直接效果是促进细菌分裂,结果是在导致细菌死亡之前,细胞数量迅速增加。在这种诱导的细胞死亡过程中,没有观察到DNA的断裂或降解。冷冻电子显微镜显示,诱导的细胞首先形成气泡,最终从死亡的细胞中释放出来。显然,气泡引发了细胞的解体,导致了细胞死亡。这些发现使我们假设,rpos表达增加会触发细胞内程序和/或导致螺旋体死亡的途径。诱导细胞死亡的潜在生物学意义可能有助于伯氏假单胞菌调节其种群以维持其在自然界中的生命周期。
RpoS, one of the two alternative σ factors in Borrelia burgdorferi, is tightly controlled by multiple regulators and, in turn, determines expression of many critical virulence factors. Here we show that increasing RpoS expression causes cell death. The immediate effect of increasing RpoS expression was to promote bacterial division and as a consequence result in a rapid increase in cell number before causing bacterial death. No DNA fragmentation or degradation was observed during this induced cell death. Cryo-electron microscopy showed induced cells first formed blebs, which were eventually released from dying cells. Apparently blebbing initiated cell disintegration leading to cell death. These findings led us to hypothesize that increasing RpoS expression triggers intracellular programs and/or pathways that cause spirochete death. The potential biological significance of induced cell death may help B. burgdorferi regulate its population to maintain its life cycle in nature.
细菌程序性细胞死亡和细菌多细胞行为。
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