Håvarstein Leiv Sigve, Martin Bernard, Johnsborg Ola, Granadel Chantal, Claverys Jean-Pierre
Laboratoire de Microbiologie et Génétique Moléculaires, UMR 5100 CNRS-Université Paul Sabatier, 118 route de Narbonne, 31062 Toulouse Cedex, France.
Mol Microbiol. 2006 Feb;59(4):1297-307. doi: 10.1111/j.1365-2958.2005.05021.x.
In 1971, Tomasz and Zanati discovered that competent pneumococci have a tendency to form aggregates when pelleted by centrifugation and resuspended in 0.01 N HCl by brief vortexing. Interestingly, no clumping was observed with parallel cultures of non-competent cells treated in the same way. We set out to elucidate the mechanism behind this striking phenomenon, and were able to show that it depends on extracellular DNA that is presumably released by so-called competence-induced cell lysis. Competence-induced cell lysis, which was first described a few years ago, seems to rely on the concerted action of several murein hydrolases. Our results confirmed and extended previous findings by showing that competence-induced aggregation is abolished in a lytA-lytC double mutant, and absolutely requires CbpD and its N-terminal CHAP amidase domain. Furthermore, we discovered a novel competence stimulating peptide (CSP)-induced immunity protein, encoded by the early competence gene comM (spr1762), which protects competent pneumococci against their own lysins. Together, the murein hydrolases and the immunity protein constitutes a CSP-controlled mechanism that allows competent pneumococci to commit fratricide by killing non-competent pneumococci sharing the same ecological niche. Through such predatory behaviour, pneumococci can get access to transforming DNA and nutrients, promote the release of virulence factors, and at the same time get rid of competitors.
1971年,托马兹(Tomasz)和扎纳蒂(Zanati)发现,感受态肺炎球菌在通过离心沉淀并经短暂涡旋重悬于0.01 N盐酸中时,有形成聚集体的倾向。有趣的是,以同样方式处理的非感受态细胞平行培养物未观察到聚集现象。我们着手阐明这一显著现象背后的机制,并能够证明它依赖于细胞外DNA,推测该DNA是由所谓的感受态诱导的细胞裂解释放的。感受态诱导的细胞裂解在几年前首次被描述,似乎依赖于几种胞壁质水解酶的协同作用。我们的结果证实并扩展了先前的发现,表明在lytA-lytC双突变体中感受态诱导的聚集被消除,并且绝对需要CbpD及其N端CHAP酰胺酶结构域。此外,我们发现了一种由早期感受态基因comM(spr1762)编码的新型感受态刺激肽(CSP)诱导的免疫蛋白,它保护感受态肺炎球菌免受自身溶素的侵害。总之,胞壁质水解酶和免疫蛋白构成了一种CSP控制的机制,使感受态肺炎球菌能够通过杀死共享相同生态位的非感受态肺炎球菌进行自相残杀。通过这种捕食行为,肺炎球菌可以获取转化DNA和营养物质,促进毒力因子的释放,同时消除竞争者。