Campoy Susana, Hervàs Anna, Busquets Núria, Erill Ivan, Teixidó Laura, Barbé Jordi
Centre de Recerca en Sanitat Animal (CReSA), Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain.
Virology. 2006 Aug 1;351(2):360-7. doi: 10.1016/j.virol.2006.04.001. Epub 2006 May 19.
Infection of Salmonella enterica with lytic mutants of either P22 or SE1 bacteriophages triggers the expression of its DNA damage-inducible SOS response through a lexA-dependent pathway. This induction of the SOS system strictly requires the presence of the bacteriophage kil gene. Accordingly, plasmid overexpression of the kil gene also promotes the S. enterica SOS network induction. Furthermore, S. enterica Gifsy prophages are induced following the infection with SE1 and P22 lytic derivatives. The observed data reveal a hitherto unknown SOS system-mediated fail-safe mechanism of resident prophages against infection with heteroimmune lytic bacteriophages and suggest a novel role for the kil family of proteins.
用P22或SE1噬菌体的裂解突变体感染肠炎沙门氏菌，会通过lexA依赖途径触发其DNA损伤诱导的SOS反应的表达。SOS系统的这种诱导严格需要噬菌体kil基因的存在。因此，kil基因的质粒过表达也会促进肠炎沙门氏菌SOS网络的诱导。此外，在用SE1和P22裂解衍生物感染后，肠炎沙门氏菌的Gifsy原噬菌体被诱导。观察到的数据揭示了一种迄今未知的SOS系统介导的常驻原噬菌体抵抗异源免疫裂解噬菌体感染的故障安全机制，并暗示了kil蛋白家族的新作用。
