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金黄色葡萄球菌的替代σ因子σB控制环境应激反应,但在小鼠脓肿模型中不控制饥饿存活或致病性。

The Staphylococcus aureus alternative sigma factor sigmaB controls the environmental stress response but not starvation survival or pathogenicity in a mouse abscess model.

作者信息

Chan P F, Foster S J, Ingham E, Clements M O

机构信息

Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield, S10 2TN, United Kingdom.

出版信息

J Bacteriol. 1998 Dec;180(23):6082-9. doi: 10.1128/JB.180.23.6082-6089.1998.

Abstract

The role of sigmaB, an alternative sigma factor of Staphylococcus aureus, has been characterized in response to environmental stress, starvation-survival and recovery, and pathogenicity. sigmaB was mainly expressed during the stationary phase of growth and was repressed by 1 M sodium chloride. A sigB insertionally inactivated mutant was created. In stress resistance studies, sigmaB was shown to be involved in recovery from heat shock at 54 degreesC and in acid and hydrogen peroxide resistance but not in resistance to ethanol or osmotic shock. Interestingly, S. aureus acquired increased acid resistance when preincubated at a sublethal pH 4 prior to exposure to a lethal pH 2. This acid-adaptive response resulting in tolerance was mediated via sigB. However, sigmaB was not vital for the starvation-survival or recovery mechanisms. sigmaB does not have a major role in the expression of the global regulator of virulence determinant biosynthesis, staphylococcal accessory regulator (sarA), the production of a number of representative virulence factors, and pathogenicity in a mouse subcutaneous abscess model. However, SarA upregulates sigB expression in a growth-phase-dependent manner. Thus, sigmaB expression is linked to the processes controlling virulence determinant production. The role of sigmaB as a major regulator of the stress response, but not of starvation-survival, is discussed.

摘要

金黄色葡萄球菌的替代西格玛因子sigmaB在应对环境压力、饥饿存活与恢复以及致病性方面的作用已得到表征。sigmaB主要在生长的稳定期表达,并受到1M氯化钠的抑制。构建了一个sigB插入失活突变体。在抗逆性研究中,sigmaB被证明参与了54摄氏度热休克后的恢复以及对酸和过氧化氢的抗性,但不参与对乙醇或渗透压休克的抗性。有趣的是,金黄色葡萄球菌在暴露于致死性pH 2之前,先在亚致死性pH 4下预孵育时,其耐酸性增强。这种导致耐受性的酸适应性反应是通过sigB介导的。然而,sigmaB对于饥饿存活或恢复机制并非至关重要。sigmaB在毒力决定因子生物合成的全局调节因子葡萄球菌辅助调节因子(sarA)的表达、多种代表性毒力因子的产生以及小鼠皮下脓肿模型中的致病性方面没有主要作用。然而,SarA以生长阶段依赖的方式上调sigB的表达。因此,sigmaB的表达与控制毒力决定因子产生的过程相关。讨论了sigmaB作为应激反应而非饥饿存活的主要调节因子的作用。

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