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hok/sok 诱导的细菌生长变化和应激反应中 FtsZ 抑制的表型指征。

Phenotypic indications of FtsZ inhibition in hok/sok-induced bacterial growth changes and stress response.

机构信息

Department of Pathology and Infectious Diseases, Royal Veterinary College, University of London, UK; Department of Veterinary Pathology and Microbiology, University of Nigeria, Nsukka, Enugu State, Nigeria.

Department of Pathology and Infectious Diseases, Royal Veterinary College, University of London, UK.

出版信息

Microb Pathog. 2018 Jan;114:393-401. doi: 10.1016/j.micpath.2017.12.023. Epub 2017 Dec 9.

Abstract

The hok/sok locus has been shown to enhance the growth of bacteria in adverse growth conditions such as high temperature, low starting-culture densities and antibiotic treatment. This is in addition to their well-established plasmid-stabilization effect via post-segregational killing of plasmid-free daughter cells. It delays the onset of growth by prolonging the lag phase of bacterial culture, and increases the rate of exponential growth when growth eventually begins. This enables the cells adapt to the prevailing growth conditions and enhance their survival in stressful conditions. These effects functionally complement defective SOS response mechanism, and appear analogous to the growth effects of FtsZ in the SOS pathway. In this study, the role of FtsZ in the hok/sok-induced changes in bacterial growth and cell division was investigated. Morphologic studies of early growth-phase cultures and cells growing under temperature stress showed elongated cells typical of FtsZ inhibition/deficiency. Both ftsZ silencing and over-expression produced comparable growth effects in control cells, and altered the growth changes observed otherwise in the hok/sok cells. These changes were diminished in SOS-deficient strain containing mutant FtsZ. The involvement of FtsZ in the hok/sok-induced growth changes may be exploited as drug target in host bacteria, which often propagate antibiotic resistance elements.

摘要

hok/sok 基因座已被证明能增强细菌在不利生长条件下的生长,如高温、低起始培养密度和抗生素处理。除了通过消除无质粒的子细胞的继代杀伤来稳定质粒的作用外,这也是如此。它通过延长细菌培养的迟滞期来延迟生长的开始,并在生长最终开始时增加指数生长的速度。这使细胞能够适应流行的生长条件,并在压力条件下增强其存活能力。这些作用在功能上补充了有缺陷的 SOS 反应机制,并且类似于 FtsZ 在 SOS 途径中的生长作用。在这项研究中,研究了 FtsZ 在 hok/sok 诱导的细菌生长和细胞分裂变化中的作用。早期生长阶段培养物和在温度胁迫下生长的细胞的形态学研究显示出典型的 FtsZ 抑制/缺乏的伸长细胞。ftsZ 沉默和过表达在对照细胞中产生了可比的生长效应,并改变了 otherwise 在 hok/sok 细胞中观察到的生长变化。在含有突变 FtsZ 的 SOS 缺陷菌株中,这些变化减少了。FtsZ 在 hok/sok 诱导的生长变化中的参与可能被用作宿主细菌的药物靶点,宿主细菌通常会传播抗生素抗性元件。

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