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炭疽芽孢杆菌的BclB糖蛋白参与芽孢外壳完整性的维持。

The BclB glycoprotein of Bacillus anthracis is involved in exosporium integrity.

作者信息

Thompson Brian M, Waller Lashanda N, Fox Karen F, Fox Alvin, Stewart George C

机构信息

471E Bond Life Sciences Center, 1201 Rollins Road, University of Missouri, Columbia, MO 65211, USA.

出版信息

J Bacteriol. 2007 Sep;189(18):6704-13. doi: 10.1128/JB.00762-07. Epub 2007 Jul 20.

DOI:10.1128/JB.00762-07
PMID:17644587
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2045162/
Abstract

Anthrax is a highly fatal disease caused by the gram-positive, endospore-forming, rod-shaped bacterium Bacillus anthracis. Spores, rather than vegetative bacterial cells, are the source of anthrax infections. Spores of B. anthracis are enclosed by a prominent loose-fitting structure called the exosporium. The exosporium is composed of a basal layer and an external hair-like nap. Filaments of the hair-like nap are made up largely of a single collagen-like glycoprotein called BclA. A second glycoprotein, BclB, has been identified in the exosporium layer. The specific location of this glycoprotein within the exosporium layer and its role in the biology of the spore are unknown. We created a mutant strain of B. anthracis DeltaSterne that carries a deletion of the bclB gene. The mutant was found to possess structural defects in the exosporium layer of the spore (visualized by electron microscopy, immunofluorescence, and flow cytometry) resulting in an exosporium that is more fragile than that of a wild-type spore and is easily lost. Immunofluorescence studies also indicated that the mutant strain produced spores with increased levels of the BclA glycoprotein accessible to the antibodies on the surface. The resistance properties of the mutant spores were unchanged from those of the wild-type spores. A bclB mutation did not affect spore germination or kinetics of spore survival within macrophages. BclB plays a key role in the formation and maintenance of the exosporium structure in B. anthracis.

摘要

炭疽病是一种由革兰氏阳性、形成芽孢的杆状细菌炭疽芽孢杆菌引起的高度致命性疾病。炭疽感染的源头是芽孢,而非繁殖期的细菌细胞。炭疽芽孢杆菌的芽孢被一种称为芽孢外膜的显著的宽松结构所包裹。芽孢外膜由一个基底层和外部毛发状绒毛组成。毛发状绒毛的细丝主要由一种名为BclA的单一胶原样糖蛋白构成。在芽孢外膜层中还鉴定出了第二种糖蛋白BclB。这种糖蛋白在芽孢外膜层中的具体位置及其在芽孢生物学中的作用尚不清楚。我们构建了一株携带bclB基因缺失的炭疽芽孢杆菌DeltaSterne突变株。通过电子显微镜、免疫荧光和流式细胞术观察发现,该突变株的芽孢外膜层存在结构缺陷,导致其芽孢外膜比野生型芽孢的更脆弱,且容易脱落。免疫荧光研究还表明,该突变株产生的芽孢表面可被抗体识别的BclA糖蛋白水平升高。突变型芽孢的抗性特性与野生型芽孢相同。bclB突变不影响芽孢萌发或巨噬细胞内芽孢存活的动力学。BclB在炭疽芽孢杆菌芽孢外膜结构的形成和维持中起关键作用。

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The ExsY protein is required for complete formation of the exosporium of Bacillus anthracis.炭疽芽孢杆菌芽孢外壳的完整形成需要ExsY蛋白。
J Bacteriol. 2006 Nov;188(21):7440-8. doi: 10.1128/JB.00639-06. Epub 2006 Aug 25.
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Transcriptional profiling of the Bacillus anthracis life cycle in vitro and an implied model for regulation of spore formation.炭疽芽孢杆菌体外生命周期的转录谱分析及芽孢形成调控的隐含模型
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Importance of nitric oxide synthase in the control of infection by Bacillus anthracis.一氧化氮合酶在炭疽芽孢杆菌感染控制中的重要性。
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Characterization of the exosporium basal layer protein BxpB of Bacillus anthracis.炭疽芽孢杆菌芽孢衣底层蛋白BxpB的特性分析
J Bacteriol. 2005 Sep;187(17):5868-76. doi: 10.1128/JB.187.17.5868-5876.2005.
9
Orientation within the exosporium and structural stability of the collagen-like glycoprotein BclA of Bacillus anthracis.炭疽芽孢杆菌类胶原蛋白糖蛋白BclA在芽孢外壳中的定位及结构稳定性
J Bacteriol. 2005 Aug;187(15):5310-7. doi: 10.1128/JB.187.15.5310-5317.2005.
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