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一般应激反应σ因子SigB的激活会阻止……中的感受态发展。 (注:原文中“in”后面缺少具体内容)

Activation of the general stress response sigma factor SigB prevents competence development in .

作者信息

Harms Marco, Michalik Stephan, Hildebrandt Petra, Schaffer Marc, Gesell Salazar Manuela, Gerth Ulf, Mäder Ulrike, van Dijl Jan Maarten, Hecker Michael, Völker Uwe, Reder Alexander

机构信息

University Medicine Greifswald, Center for Functional Genomics of Microbes, Interfaculty Institute for Genetics and Functional Genomics, Greifswald, Germany.

University of Greifswald, Center for Functional Genomics of Microbes, Institute of Microbiology, Greifswald, Germany.

出版信息

mBio. 2024 Dec 11;15(12):e0227424. doi: 10.1128/mbio.02274-24. Epub 2024 Oct 29.

DOI:10.1128/mbio.02274-24
PMID:39470193
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11633097/
Abstract

UNLABELLED

Seemingly simple bacteria mount intricate adaptive responses when exposed to physical stress or nutrient limitation, and the activation of these responses is governed by complex signal transduction networks. Upon entry into the stationary growth phase, the soil bacterium may develop natural competence, form biofilms or stress-resistant cells, or ultimately trigger a cellular differentiation program leading to spore formation. Master regulators, such as Spo0A, ComK, SinR, and SigB, constantly monitor the bacterium's environment and then determine appropriate adaptive responses. Here, we show that exposure of to visible light and other stresses triggers a general stress response-dependent block in competence development. SigB serves as an "emergency system" to silence inappropriate expression of an alternative developmental program in the face of unfavorable conditions. In particular, we document a stress-dependent molecular mechanism that prevents accumulation of the central competence regulator ComK via expression of a SigB-driven antisense RNA (, S365) which is part of a noncontiguous operon.

IMPORTANCE

exhibits a large number of different specific and general adaptation reactions, which need to be well balanced to sustain survival under largely unfavorable conditions. Under specific conditions, natural competence develops, which enables to actively take up exogenous DNA to integrate it into its own genome. In contrast to this specific adaptation, the general stress response is induced by a variety of exogenous stress and starvation stimuli, providing comprehensive protection and enabling survival of vegetative cells. In the present work, we reveal the molecular basis for the interconnection of these two important responses in the regulatory network. We describe that the master regulator of the general stress response SigB is activated by physiological stress stimuli, including daylight and ethanol stress, leading to the inactivation of the competence master regulator ComK by transcriptional anti-sense regulation, showing a strict hierarchy of adaptational responses under severe stress.

摘要

未标记

看似简单的细菌在受到物理应激或营养限制时会产生复杂的适应性反应,而这些反应的激活由复杂的信号转导网络控制。进入稳定生长期后,这种土壤细菌可能会发展出自然感受态、形成生物膜或抗应激细胞,或者最终触发导致孢子形成的细胞分化程序。主调控因子,如Spo0A、ComK、SinR和SigB,不断监测细菌的环境,然后确定适当的适应性反应。在这里,我们表明,暴露于可见光和其他应激会触发依赖于一般应激反应的感受态发育阻滞。SigB作为一种“应急系统”,在不利条件下沉默替代发育程序的不适当表达。特别是,我们记录了一种依赖应激的分子机制,该机制通过表达SigB驱动的反义RNA(,S365)来阻止中央感受态调控因子ComK的积累,该反义RNA是一个不连续操纵子的一部分。

重要性

表现出大量不同的特异性和一般性适应反应,在很大程度上不利的条件下需要很好地平衡这些反应以维持生存。在特定条件下,会发展出自然感受态,这使得能够主动摄取外源DNA并将其整合到自身基因组中。与这种特异性适应相反,一般应激反应由多种外源应激和饥饿刺激诱导,提供全面保护并使营养细胞能够存活。在本研究中,我们揭示了调控网络中这两种重要反应相互联系的分子基础。我们描述了一般应激反应的主调控因子SigB被包括日光和乙醇应激在内的生理应激刺激激活,导致通过转录反义调控使感受态主调控因子ComK失活,显示出在严重应激下适应反应的严格层次结构。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/a0d6231b3f6e/mbio.02274-24.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/034043b4c44b/mbio.02274-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/af5db0428b20/mbio.02274-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/1602abc30e44/mbio.02274-24.f003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/24f5f0f6c812/mbio.02274-24.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/39f88f674ff7/mbio.02274-24.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/a0d6231b3f6e/mbio.02274-24.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/034043b4c44b/mbio.02274-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/af5db0428b20/mbio.02274-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/1602abc30e44/mbio.02274-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/6163be625b5a/mbio.02274-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/24f5f0f6c812/mbio.02274-24.f005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72bf/11633097/a0d6231b3f6e/mbio.02274-24.f007.jpg

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