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spoIID 缺失会降低炭疽芽孢杆菌的孢子形成能力,增加细胞外蛋白水解活性和毒力。

Disruption of SpoIIID decreases sporulation, increases extracellular proteolytic activity and virulence in Bacillus anthracis.

机构信息

State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Biotechnology, 20 Dongdajie Street, Fengtai District, Beijing, 100071, China.

College of Food Science and Technology, Shanghai Engineering Research Center of Aquatic-Product Processing & Preservation, Shanghai Ocean University, No. 999, Huchenghuan Road, Shanghai, 201306, PR China.

出版信息

Biochem Biophys Res Commun. 2019 Jun 4;513(3):651-656. doi: 10.1016/j.bbrc.2019.04.056. Epub 2019 Apr 11.

DOI:10.1016/j.bbrc.2019.04.056
PMID:30982579
Abstract

Endospores are important for maintenance of the B. anthracis lifecycle and necessary for its effective spread between hosts. Our experiments with B. anthracis showed that disruption of SpoIIID results in a spore formation defect, as determined by heat resistance assays and microscopic assessment. We further found complete engulfment by the ΔspoIIID mutant strain by membrane morphology staining but no synthesis of the clarity coat and exosporium by transmission electron microscopy. Reduced transcription and expression of small acid-soluble spore protein(sasP-2) and the spore development associated genes (σ, gerE and cotE) in the mother cell were found in the ΔspoIIID strain, suggesting that the spore formation defect in B. anthracis A16R is related to decreased transcription and expression of these genes. Extracellular protease and virulence enhancement in the ΔspoIIID strain may be related to the elevation of metalloproteinases (TasA and Camelysin) levels. Our findings pave the way for further research on the regulation network of sporulation, survival and virulence in these two morphological forms of B. anthracis.

摘要

芽孢是炭疽杆菌生命周期维持的重要因素,也是其在宿主间有效传播所必需的。我们的炭疽杆菌实验表明,spoIID 基因的破坏导致芽孢形成缺陷,这可以通过耐热性测定和显微镜评估来确定。我们进一步通过细胞膜形态染色发现,ΔspoIIID 突变菌株完全被吞噬,但透射电子显微镜显示没有清晰涂层和外孢囊的合成。在 ΔspoIIID 菌株中,小酸溶性孢子蛋白(sasP-2)和与孢子发育相关的基因(σ、gerE 和 cotE)的转录和表达减少,表明炭疽杆菌 A16R 的芽孢形成缺陷与这些基因的转录和表达减少有关。ΔspoIIID 菌株中细胞外蛋白酶和毒力增强可能与金属蛋白酶(TasA 和 Camelysin)水平升高有关。我们的研究结果为进一步研究这两种炭疽杆菌形态的孢子形成、生存和毒力的调控网络铺平了道路。

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Disruption of SpoIIID decreases sporulation, increases extracellular proteolytic activity and virulence in Bacillus anthracis.spoIID 缺失会降低炭疽芽孢杆菌的孢子形成能力,增加细胞外蛋白水解活性和毒力。
Biochem Biophys Res Commun. 2019 Jun 4;513(3):651-656. doi: 10.1016/j.bbrc.2019.04.056. Epub 2019 Apr 11.
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Maintaining the transcription factor SpoIIID level late during sporulation causes spore defects in Bacillus subtilis.在枯草芽孢杆菌的芽孢形成后期维持转录因子SpoIIID的水平会导致芽孢缺陷。
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The stringent response of Bacillus anthracis contributes to sporulation but not to virulence.炭疽芽孢杆菌的严谨反应有助于芽孢形成,但与毒力无关。
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Effect of the spoIIID mutation on mother cell lysis in Bacillus thuringiensis.spoIIID 突变对苏云金芽孢杆菌母细胞裂解的影响。
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Characterization of a Bacillus anthracis spore coat-surface protein that influences coat-surface morphology.一种影响芽孢表面形态的炭疽芽孢杆菌芽孢表面蛋白的特性分析。
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The BclB glycoprotein of Bacillus anthracis is involved in exosporium integrity.炭疽芽孢杆菌的BclB糖蛋白参与芽孢外壳完整性的维持。
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One perturbation of the mother cell gene regulatory network suppresses the effects of another during sporulation of Bacillus subtilis.在枯草芽孢杆菌的孢子形成过程中,母细胞基因调控网络的一种扰动会抑制另一种扰动的影响。
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Fate of the SpoIIID switch protein during Bacillus subtilis sporulation depends on the mother-cell sigma factor, sigma K.枯草芽孢杆菌芽孢形成过程中SpoIIID开关蛋白的命运取决于母细胞σ因子σK。
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