Garcia Erin C, Perault Andrew I, Marlatt Sara A, Cotter Peggy A
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
Proc Natl Acad Sci U S A. 2016 Jul 19;113(29):8296-301. doi: 10.1073/pnas.1606323113. Epub 2016 Jun 22.
In prokaryotes and eukaryotes, cell-cell communication and recognition of self are critical to coordinate multicellular functions. Although kin and kind discrimination are increasingly appreciated to shape naturally occurring microbe populations, the underlying mechanisms that govern these interbacterial interactions are insufficiently understood. Here, we identify a mechanism of interbacterial signal transduction that is mediated by contact-dependent growth inhibition (CDI) system proteins. CDI systems have been characterized by their ability to deliver a polymorphic protein toxin into the cytoplasm of a neighboring bacterium, resulting in growth inhibition or death unless the recipient bacterium produces a corresponding immunity protein. Using the model organism Burkholderia thailandensis, we show that delivery of a catalytically active CDI system toxin to immune (self) bacteria results in gene expression and phenotypic changes within the recipient cells. Termed contact-dependent signaling (CDS), this response promotes biofilm formation and other community-associated behaviors. Engineered strains that are isogenic with B. thailandensis, except the DNA region encoding the toxin and immunity proteins, did not display CDS, whereas a strain of Burkholderia dolosa producing a nearly identical toxin-immunity pair induced signaling in B. thailandensis Our data indicate that bcpAIOB loci confer dual benefits; they direct antagonism toward non-self bacteria and promote cooperation between self bacteria, with self being defined by the bcpAIOB allele and not by genealogic relatedness.
在原核生物和真核生物中，细胞间通讯和自我识别对于协调多细胞功能至关重要。尽管亲缘和同类识别对塑造自然存在的微生物群体的作用越来越受到重视，但调控这些细菌间相互作用的潜在机制仍未得到充分理解。在此，我们鉴定出一种由接触依赖性生长抑制（CDI）系统蛋白介导的细菌间信号转导机制。CDI系统的特点是能够将一种多态性蛋白毒素传递到邻近细菌的细胞质中，导致生长抑制或死亡，除非受体细菌产生相应的免疫蛋白。利用模式生物泰国伯克霍尔德菌，我们发现将具有催化活性的CDI系统毒素传递给免疫（自身）细菌会导致受体细胞内的基因表达和表型变化。这种反应被称为接触依赖性信号传导（CDS），它促进生物膜形成和其他与群体相关的行为。与泰国伯克霍尔德菌等基因的工程菌株，除了编码毒素和免疫蛋白的DNA区域外，不显示CDS，而产生几乎相同毒素-免疫对的多洛沙伯克霍尔德菌菌株在泰国伯克霍尔德菌中诱导信号传导。我们的数据表明，bcpAIOB基因座具有双重益处；它们对非自身细菌产生拮抗作用，并促进自身细菌之间的合作，自身由bcpAIOB等位基因定义，而非谱系相关性。
