Regulation of sialidase production in Clostridium perfringens by the orphan sensor histidine kinase ReeS.
Regulation of sialidase production in Clostridium perfringens by the orphan sensor histidine kinase ReeS.
复制标题
通过孤儿传感器组氨酸激酶REES调节唾液酸酶孔梭状芽胞杆菌的产生。
DOI：
10.1371/journal.pone.0073525
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Rood JI
中科院分区：
文献类型：
--
作者：
Hiscox TJ;Harrison PF;Chakravorty A;Choo JM;Ohtani K;Shimizu T;Cheung JK;Rood JI
产气荚膜梭菌在自然界中普遍存在，并且经常被发现作为人和动物胃肠道的寄生虫。它是梭菌性肌坏死或气性坏疽的主要病原体，这是一种严重感染，由于一种或多种强效细胞外毒素的作用而导致广泛的组织坏死。α-毒素和产气荚膜梭菌溶素O是参与气性坏疽发病的主要胞外毒素，但组织毒力强的C.产气荚膜杆菌（例如菌株13）也产生许多降解酶，例如胶原酶、透明质酸酶、唾液酸酶和半胱氨酸蛋白酶、α-梭菌蛋白酶。许多这些毒素的产生直接或间接地受全球VirSR双组分信号转导系统的调节。通过分离染色体突变体和进行微阵列分析，我们已经确定了一个孤儿传感器组氨酸激酶，我们已经命名为ReeS（调节器的胞外酶传感器）。在reeS突变体中，唾液酸酶基因nanI和nanJ的表达下调。由于与野生型reeS基因互补恢复nanI和nanJ表达到野生型水平，如定量逆转录PCR和唾液酸酶测定所示，我们得出结论，ReeS正调控这些唾液酸酶基因的表达。然而，reeS基因突变对小鼠肌坏死模型的毒力没有显著影响。C.先前已显示产气荚膜杆菌受VirSR系统和RevR两者调节。在本报告中，我们分析了一种以前未知的传感器组胺酸激酶ReeS，并表明它也参与控制唾液酸酶基因的表达，从而为控制C中唾液酸酶产生的调节网络增加了进一步的复杂性。产气荚膜杆菌
Clostridium perfringens is ubiquitous in nature and is often found as a commensal of the human and animal gastrointestinal tract. It is the primary etiological agent of clostridial myonecrosis, or gas gangrene, a serious infection that results in extensive tissue necrosis due to the action of one or more potent extracellular toxins. α-toxin and perfringolysin O are the major extracellular toxins involved in the pathogenesis of gas gangrene, but histotoxic strains of C. perfringens, such as strain 13, also produce many degradative enzymes such as collagenases, hyaluronidases, sialidases and the cysteine protease, α-clostripain. The production of many of these toxins is regulated either directly or indirectly by the global VirSR two-component signal transduction system. By isolating a chromosomal mutant and carrying out microarray analysis we have identified an orphan sensor histidine kinase, which we have named ReeS (regulator of extracellular enzymes sensor). Expression of the sialidase genes nanI and nanJ was down-regulated in a reeS mutant. Since complementation with the wild-type reeS gene restored nanI and nanJ expression to wild-type levels, as shown by quantitative reverse transcription-PCR and sialidase assays we concluded that ReeS positively regulates the expression of these sialidase genes. However, mutation of the reeS gene had no significant effect on virulence in the mouse myonecrosis model. Sialidase production in C. perfringens has been previously shown to be regulated by both the VirSR system and RevR. In this report, we have analyzed a previously unknown sensor histidine kinase, ReeS, and have shown that it also is involved in controlling the expression of sialidase genes, adding further complexity to the regulatory network that controls sialidase production in C. perfringens.
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影响因子：
30.3
作者：
Martens EC;Chiang HC;Gordon JI
通讯作者：
Gordon JI
影响因子：
3.8
作者：
Awad, MM;Ellemor, DM;Rood, JI
通讯作者：
Rood, JI
影响因子：
3.2
作者：
BaThein, W;Lyristis, M;Shimizu, T
通讯作者：
Shimizu, T
影响因子：
4.8
作者：
Flores-Díaz, M;Alape-Girón, A;Titball, R
通讯作者：
Titball, R
DOI：
10.1073/pnas.0909950107
发表时间：
2010-03-02
影响因子：
11.1
作者：
Menke, Matt;Berger, Bonnie;Cowen, Lenore
通讯作者：
Cowen, Lenore