Thomas Vinai Chittezham, Hiromasa Yasuaki, Harms Nathan, Thurlow Lance, Tomich John, Hancock Lynn E
Division of Biology, Kansas State University, 116 Ackert Hall, Manhattan, KS, USA.
Mol Microbiol. 2009 May;72(4):1022-36. doi: 10.1111/j.1365-2958.2009.06703.x. Epub 2009 Apr 21.
Extracellular DNA (eDNA), a by-product of cell lysis, was recently established as a critical structural component of the Enterococcus faecalis biofilm matrix. Here, we describe fratricide as the governing principle behind gelatinase (GelE)-mediated cell death and eDNA release. GFP reporter assays confirmed that GBAP (gelatinase biosynthesis-activating pheromone) quorum non-responders (GelE-SprE-) were a minority subpopulation of prey cells susceptible to the targeted fratricidal action of the quorum responsive predatorial majority (GelE+SprE+). The killing action is dependent on GelE, and the GelE producer population is protected from self-destruction by the co-production of SprE as an immunity protein. Targeted gene inactivation and protein interaction studies demonstrate that extracellular proteases execute their characteristic effects following downstream interactions with the primary autolysin, AtlA. Finally, we address a mechanism by which GelE and SprE may modify the cell wall affinity of proteolytically processed AtlA resulting in either a pro- or anti-lytic outcome.
细胞外DNA（eDNA）是细胞裂解的副产物，最近被确定为粪肠球菌生物膜基质的关键结构成分。在此，我们将自相残杀描述为明胶酶（GelE）介导的细胞死亡和eDNA释放背后的主导原则。绿色荧光蛋白（GFP）报告基因检测证实，群体感应无反应者（GelE-SprE-）是易受群体感应反应性捕食多数群体（GelE+SprE+）靶向自相残杀作用影响的少数猎物细胞亚群。杀伤作用依赖于GelE，而产生GelE的群体通过共同产生作为免疫蛋白的SprE来防止自我毁灭。靶向基因失活和蛋白质相互作用研究表明，细胞外蛋白酶在与主要自溶素AtlA发生下游相互作用后发挥其特征性作用。最后，我们探讨了一种机制，通过该机制GelE和SprE可能会改变经蛋白水解处理的AtlA对细胞壁的亲和力，从而导致促裂解或抗裂解结果。
