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AtxA通过acpA和一个新发现的调节因子acpB来控制炭疽芽孢杆菌的荚膜合成。

atxA controls Bacillus anthracis capsule synthesis via acpA and a newly discovered regulator, acpB.

作者信息

Drysdale Melissa, Bourgogne Agathe, Hilsenbeck Susan G, Koehler Theresa M

机构信息

Department of Microbiology and Molecular Genetics, The University of Texas-Houston Health Science Center, Houston, Texas 77030, USA.

出版信息

J Bacteriol. 2004 Jan;186(2):307-15. doi: 10.1128/JB.186.2.307-315.2004.

DOI:10.1128/JB.186.2.307-315.2004
PMID:14702298
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC305762/
Abstract

Two regulatory genes, acpA and atxA, have been reported to control expression of the Bacillus anthracis capsule biosynthesis operon capBCAD. The atxA gene is located on the virulence plasmid pXO1, while pXO2 carries acpA and the cap genes. acpA has been viewed as the major regulator of the cap operon because it is essential for capsule gene expression in a pXO1(-) pXO2(+) strain. atxA is essential for toxin gene transcription but has also been implicated in control of the cap genes. The molecular functions of the regulatory proteins are unknown. We examined cap gene expression in a genetically complete pXO1(+) pXO2(+) strain. Our results indicate that another pXO2 gene, acpB (previously called pXO2-53; accession no. NC002146.1:49418-50866), has a role in cap expression. The predicted amino acid sequence of AcpB is 62% similar to that of AcpA and 50% similar to that of AtxA. Assessment of cap gene transcription revealed that cap expression was not affected in a pXO1(+) pXO2(+) acpB-null mutant and was slightly reduced in an isogenic acpA mutant. However, cap gene expression was abolished in an acpA acpB double mutant. Microscopic examination of capsule synthesis by the mutants corroborated these findings. acpA and acpB expression is controlled by atxA; capsule synthesis and transcription of acpA and acpB were markedly reduced in an atxA mutant. The data suggest that, in a strain containing both virulence plasmids, atxA is the major regulator of capsule synthesis and controls capBCAD expression indirectly, via positive regulation of acpA and acpB.

摘要

据报道,两个调控基因acpA和atxA可控制炭疽芽孢杆菌荚膜生物合成操纵子capBCAD的表达。atxA基因位于毒力质粒pXO1上,而pXO2携带acpA和cap基因。acpA被视为cap操纵子的主要调控因子,因为它对于pXO1(-) pXO2(+)菌株中的荚膜基因表达至关重要。atxA对于毒素基因转录必不可少,但也与cap基因的调控有关。这些调控蛋白的分子功能尚不清楚。我们检测了基因完整的pXO1(+) pXO2(+)菌株中的cap基因表达。我们的结果表明,另一个pXO2基因acpB(以前称为pXO2-53;登录号NC002146.1:49418-50866)在cap表达中发挥作用。AcpB的预测氨基酸序列与AcpA的相似性为62%,与AtxA的相似性为50%。对cap基因转录的评估显示,cap表达在pXO1(+) pXO2(+) acpB缺失突变体中未受影响,而在同基因acpA突变体中略有降低。然而,cap基因表达在acpA acpB双突变体中被消除。对突变体荚膜合成的显微镜检查证实了这些发现。acpA和acpB的表达受atxA控制;在atxA突变体中,荚膜合成以及acpA和acpB的转录显著降低。数据表明,在同时含有两种毒力质粒的菌株中,atxA是荚膜合成的主要调控因子,并通过对acpA和acpB的正调控间接控制capBCAD的表达。

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