plcR papR-independent expression of anthrolysin O by Bacillus anthracis.

plcR papR-independent expression of anthrolysin O by Bacillus anthracis.
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炭疽芽孢杆菌不依赖 plcR papR 表达 anthrolysin O。

DOI:
10.1128/jb.00525-06
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发表时间:
2006
影响因子:
3.2
通讯作者:
Koehler,TheresaM
Koehler,TheresaM
中科院分区:
生物学3区
文献类型:
--
作者:
Ross,CanaL;Koehler,TheresaM

文献摘要

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胆固醇依赖性溶细胞素(Cholesterol-dependent cytolysins,CDC)是一种分泌型、致孔性毒素,与多种革兰氏阳性菌的致病性有关,炭疽杆菌在适当的培养条件下可产生蒽溶素O(anthrolysin O,ALO),这种CDC对培养上清液的溶血活性起主要作用。cereusandB.苏云金芽孢杆菌(B. thuringiensis)和苏云金芽孢杆菌(B.炭疽杆菌产生与ALO具有显著氨基酸序列同源性的CDC。B的转录。cereusandB.苏云金杆菌CDC基因由PlcR控制,PlcR是一种转录调节因子,需要来自papR基因产物的五肽与共有序列(PlcR盒)结合并转录激活下游基因。在B之前有一个PlcR框。anthracis alogene和B.炭疽基因组包含三个plcR样基因,其中一个含有无义突变,预计会导致截短的无功能蛋白质。我们在B.炭疽感染的小鼠,表明体内基因表达。批量培养中的alotranscription分析揭示了位于PlcR框和翻译起点之间的潜在转录起点。然而,稳态水平ofalotranscripts和ALO蛋白不受删除papR或破坏的PlcR框。我们的数据表明,尽管B.由于炭疽杆菌的基因启动子区含有PlcR盒,因此aloR的表达不依赖于这个调控系统。
Cholesterol-dependent cytolysins (CDCs) are secreted, pore-forming toxins that are associated with pathogenesis in a variety of gram-positive bacteria.Bacillus anthracisproduces anthrolysin O (ALO), a CDC that is largely responsible for the hemolytic activity of culture supernates when the bacterium is cultured in appropriate conditions.B. cereusandB. thuringiensis, species closely related toB. anthracis, produce CDCs with significant amino acid sequence homology to ALO. Transcription of theB. cereusandB. thuringiensisCDC genes is controlled by PlcR, a transcription regulator that requires a pentapeptide derived from thepapRgene product for binding to a consensus sequence (PlcR box) and transcriptional activation of downstream genes. A PlcR box precedes theB. anthracis alogene, and theB. anthracisgenome contains threeplcR-like genes, one of which harbors a nonsense mutation that is predicted to result in a truncated, nonfunctional protein. We detected mRNA ofalo,papR, and the threeplcR-like genes in spleens ofB. anthracis-infected mice, indicating gene expression in vivo. Analysis ofalotranscription in batch culture revealed a potential transcription start located between the PlcR box and the translational start. Nevertheless, steady-state levels ofalotranscripts and ALO protein were unaffected by deletion ofpapRor disruption of the PlcR box. Our data indicate that despite the presence of the transcriptionally activeplcRandpapRgenes inB. anthracisand a PlcR box in the promoter region of thealogene,aloexpression is independent of this control system.