Carbon catabolite repression of type IV pilus-dependent gliding motility in the anaerobic pathogen Clostridium perfringens
Carbon catabolite repression of type IV pilus-dependent gliding motility in the anaerobic pathogen Clostridium perfringens
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DOI：
10.1128/jb.01407-07
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发表时间：
2008-01-01
影响因子：
3.2
通讯作者：
Sarker, Mahfuzur R.
中科院分区：
文献类型：
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作者：
Mendez, Marcelo;Huang, I-Hsiu;Sarker, Mahfuzur R.
产气荚膜梭菌是一种厌氧、革兰氏阳性、孢子形成细菌，可引起人类和动物严重的组织毒性和胃肠道疾病。对三种可用的基因组测序的C.产气荚膜杆菌菌株（13、SM 101和ATCC 13124）显示编码鞭毛蛋白的基因和参与趋化性的基因不存在。然而，这些菌株表现出IV型菌毛（TFP）依赖的滑行运动。由于碳分解代谢物调节与控制不同的细菌行为有关，我们研究了葡萄糖和其他易代谢的碳水化合物对C。产气荚膜梭菌滑动运动我们的研究结果表明，碳分解代谢物调节构成了一个重要的生理调节机制，减少了大量无关的人类和动物源性致病性C的滑行运动的profability。产气荚膜杆菌菌株。葡萄糖对滑行发育产生强烈的剂量依赖性抑制，而不影响营养生长。最大的滑动抑制观察到葡萄糖浓度（1%）以前报道也抑制其他重要的行为在C。产气荚膜杆菌，如孢子发育。在葡萄糖的存在下，滑行发展的抑制是由于，至少部分是由于抑制的基因pilT和pilD，其产品是必需的TFP依赖的滑行能力。葡萄糖对pilT和pilD表达的抑制作用受关键调节蛋白CcpA（分解代谢物控制蛋白A）的控制。ccpA基因敲除的C.在1%葡萄糖存在下，产气荚膜杆菌突变株恢复了pilT和pilD的表达以及滑行能力。在引入含有野生型ccpA拷贝的互补质粒后，ccpA突变株的滑行运动的碳分解代谢物阻遏得以恢复。这些结果表明，CcpA在协调碳分解代谢物调节对C.产气荚膜梭菌滑动运动此外，我们发现了一个新的积极作用，CcpA在pilT和pilD的表达和滑行能力的情况下，分解代谢物的调节。本文结合C.产气荚膜杆菌
Clostridium perfringens is an anaerobic, gram-positive, spore-forming bacterium responsible for the production of severe histotoxic and gastrointestinal diseases in humans and animals. In silico analysis of the three available genome-sequenced C. perfringens strains (13, SM101, and ATCC13124) revealed that genes that encode flagellar proteins and genes involved in chemotaxis are absent. However, those strains exhibit type IV pilus (TFP)-dependent gliding motility. Since carbon catabolite regulation has been implicated in the control of different bacterial behaviors, we investigated the effects of glucose and other readily metabolized carbohydrates on C. perfringens gliding motility. Our results demonstrate that carbon catabolite regulation constitutes an important physiological regulatory mechanism that reduces the proficiencies of the gliding motilities of a large number of unrelated human- and animal-derived pathogenic C. perfringens strains. Glucose produces a strong dose-dependent inhibition of gliding development without affecting vegetative growth. Maximum gliding inhibition was observed at a glucose concentration (1%) previously reported to also inhibit other important behaviors in C. perfringens, such as spore development. The inhibition of gliding development in the presence of glucose was due, at least in part, to the repression of the genes pilT and pilD, whose products are essential for TFP-dependent gliding proficiency. The inhibitory effects of glucose on pilT and pilD expression were under the control of the key regulatory protein CcpA (catabolite control protein A). The deficiency in CcpA activity of a ccpA knockout C. perfringens mutant strain restored the expressions of pilT and pilD and gliding proficiency in the presence of 1% glucose. The carbon catabolite repression of the gliding motility of the ccpA mutant strain was restored after the introduction of a complementing plasmid harboring a wild-type copy of ccpA. These results point to a central role for CcpA in orchestrating the negative effect of carbon catabolite regulation on C. perfringens gliding motility. Furthermore, we discovered a novel positive role for CcpA in pilT and pilD expression and gliding proficiency in the absence of catabolite regulation. Carbon catabolite repression of gliding motility and the dual role of CcpA, either as repressor or as activator of gliding, are analyzed in the context of the different social behaviors and diseases produced by C. perfringens.