Enomoto Shinichiro, Chari Abhishek, Clayton Adam Larsen, Dale Colin
Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112, USA.
Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112, USA.
Cell Host Microbe. 2017 May 10;21(5):629-636.e5. doi: 10.1016/j.chom.2017.04.003.
Sodalis praecaptivus is a close relative and putative environmental progenitor of the widely distributed, insect-associated, Sodalis-allied symbionts. Here we show that mutant strains of S. praecaptivus that lack genetic components of a quorum-sensing (QS) apparatus have a rapid and potent killing phenotype following microinjection into an insect host. Transcriptomic and genetic analyses indicate that insect killing occurs as a consequence of virulence factors, including insecticidal toxins and enzymes that degrade the insect integument, which are normally repressed by QS at high infection densities. This method of regulation suggests that virulence factors are only utilized in early infection to initiate the insect-bacterial association. Once bacteria reach sufficient density in host tissues, the QS circuit represses expression of these harmful genes, facilitating a long-lasting and benign association. We discuss the implications of the functionality of this QS system in the context of establishment and evolution of mutualistic relationships involving these bacteria.
前捕获索氏菌是广泛分布的、与昆虫相关的、索氏菌属共生菌的近亲及假定环境祖先。在此我们表明，缺乏群体感应（QS）装置遗传成分的前捕获索氏菌突变株在显微注射到昆虫宿主后具有快速且强效的杀伤表型。转录组学和遗传学分析表明，昆虫死亡是由毒力因子导致的，包括杀虫毒素和降解昆虫体表的酶，这些毒力因子在高感染密度下通常会被群体感应抑制。这种调控方式表明，毒力因子仅在感染早期用于启动昆虫与细菌的关联。一旦细菌在宿主组织中达到足够密度，群体感应回路就会抑制这些有害基因的表达，从而促进持久且良性的关联。我们在涉及这些细菌的互利关系的建立和进化背景下讨论了这种群体感应系统功能的影响。
