Ruhe Zachary C, Nguyen Josephine Y, Chen Annette J, Leung Nicole Y, Hayes Christopher S, Low David A
Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, Santa Barbara, California, United States of America.
Biomolecular Science and Engineering Program, University of California, Santa Barbara, Santa Barbara, California, United States of America.
PLoS Genet. 2016 Jun 29;12(6):e1006145. doi: 10.1371/journal.pgen.1006145. eCollection 2016 Jun.
Contact-dependent growth inhibition (CDI) systems are widespread amongst Gram-negative bacteria where they play important roles in inter-cellular competition and biofilm formation. CDI+ bacteria use cell-surface CdiA proteins to bind neighboring bacteria and deliver C-terminal toxin domains. CDI+ cells also express CdiI immunity proteins that specifically neutralize toxins delivered from adjacent siblings. Genomic analyses indicate that cdi loci are commonly found on plasmids and genomic islands, suggesting that these Type 5 secretion systems are spread through horizontal gene transfer. Here, we examine whether CDI toxin and immunity activities serve to stabilize mobile genetic elements using a minimal F plasmid that fails to partition properly during cell division. This F plasmid is lost from Escherichia coli populations within 50 cell generations, but is maintained in ~60% of the cells after 100 generations when the plasmid carries the cdi gene cluster from E. coli strain EC93. By contrast, the ccdAB "plasmid addiction" module normally found on F exerts only a modest stabilizing effect. cdi-dependent plasmid stabilization requires the BamA receptor for CdiA, suggesting that plasmid-free daughter cells are inhibited by siblings that retain the CDI+ plasmid. In support of this model, the CDI+ F plasmid is lost rapidly from cells that carry an additional cdiI immunity gene on a separate plasmid. These results indicate that plasmid stabilization occurs through elimination of non-immune cells arising in the population via plasmid loss. Thus, genetic stabilization reflects a strong selection for immunity to CDI. After long-term passage for more than 300 generations, CDI+ plasmids acquire mutations that increase copy number and result in 100% carriage in the population. Together, these results show that CDI stabilizes genetic elements through a toxin-mediated surveillance mechanism in which cells that lose the CDI system are detected and eliminated by their siblings.
接触依赖性生长抑制(CDI)系统在革兰氏阴性菌中广泛存在,在细胞间竞争和生物膜形成中发挥重要作用。携带CDI的细菌利用细胞表面的CdiA蛋白结合邻近细菌,并传递C末端毒素结构域。携带CDI的细胞还表达CdiI免疫蛋白,可特异性中和相邻菌传递的毒素。基因组分析表明,cdi基因座常见于质粒和基因组岛,这表明这些5型分泌系统通过水平基因转移传播。在这里,我们使用一个在细胞分裂过程中不能正确分配的最小F质粒,研究CDI毒素和免疫活性是否有助于稳定移动遗传元件。这种F质粒在50个细胞世代内从大肠杆菌群体中丢失,但当质粒携带大肠杆菌菌株EC93的cdi基因簇时,在100代后约60%的细胞中得以维持。相比之下,通常存在于F质粒上的ccdAB“质粒成瘾”模块仅发挥适度的稳定作用。依赖cdi的质粒稳定需要CdiA的BamA受体,这表明不含质粒的子细胞会被保留CDI+质粒的相邻菌抑制。支持这一模型的是,携带CDI+的F质粒会从在另一个质粒上携带额外cdiI免疫基因的细胞中迅速丢失。这些结果表明,质粒稳定是通过消除群体中因质粒丢失而产生的非免疫细胞来实现的。因此,遗传稳定反映了对CDI免疫的强烈选择。经过300多代的长期传代后,携带CDI的质粒获得了增加拷贝数的突变,并导致群体中100%的携带率。总之,这些结果表明,CDI通过一种毒素介导的监测机制稳定遗传元件,在这种机制中,失去CDI系统的细胞会被其相邻菌检测并消除。