Identification of a contact-dependent growth inhibition system in the probiotic Escherichia coli Nissle 1917
Identification of a contact-dependent growth inhibition system in the probiotic Escherichia coli Nissle 1917
复制标题
益生菌大肠杆菌 Nissle 中接触依赖性生长抑制系统的鉴定，1917 年。
DOI：
10.1093/femsle/fny102
复制
发表时间：
2018-06-01
影响因子：
2.1
通讯作者：
Zhang, Youming
中科院分区：
文献类型：
--
作者：
Chen, Hanna;Fang, Qian;Zhang, Youming
接触依赖性生长抑制 (CDI) 是一种竞争机制，已在伯克霍尔德氏菌、迪克氏菌、大肠杆菌和耶尔森氏菌等多种菌株中得到鉴定。经典的CDI系统包含三个基因：cdiB、cdiA和cdiI。 cdiB 基因编码的 CdiB 是一种保守的 f3 桶蛋白，是 CdiA 输出所必需的。 cdiA基因编码的CdiA蛋白包括保守的N端结构域和可变的C端毒性结构域(CdiA-CT)。免疫蛋白 CdiI 结合毒素蛋白 CdiA-CT 并使之失活。在这里，我们鉴定了两个 CDI 系统，一个完整的 cdiBAI 操纵子，由于意外突变而具有截短的 CdiB，以及益生菌大肠杆菌 Nissle 1917 (EcN) 基因组中的“孤儿”cdiA-CT/cdil 模块。来自 EcN 的两种 CdiA-CT 在转移到大肠杆菌 DH5a 中时均表现出自抑制活性，并且氨基酸残基的连续删除导致产生最有效的 CdiA-CT 突变体。 Cdil 中和了 CdiA 的毒性活性，如之前报道的那样，Cdil 是免疫蛋白。总之，这是第一篇关于功能性 CDI 系统存在于益生菌 EcN 中的报道，可能为益生菌 EcN 在肠道微环境中提供潜在的竞争机制。
Contact-dependent growth inhibition (CDI) is a type of competitive mechanisms and has been identified in various strains including Burkholderia, Dickeya, E. coli and Yersinia. Classical CDI systems contain three genes, cdiB, cdiA and cdiI. CdiB encoded by cdiB gene is a conserved f3-barrel protein and required for export of CdiA. CdiA protein encoded by cdiA gene includes a conserved N-terminal domain and variable C-terminal toxic domain (CdiA-CT). Immunity protein CdiI binds and inactivates toxin protein CdiA-CT. Here, we identified two CDI systems, an intact cdiBAI operon with a truncated CdiB due to an unexpected mutation and an 'orphan' cdiA-CT/cdil module in the probiotic Escherichia coli Nissle 1917 (EcN) genome. Both CdiA-CTs from EcN showed auto-inhibition activity when transferring into E. coli DH5a, as well the sequential deletion of amino acid residues resulted in the generation of the most potent mutant of CdiA-CT. Cdil neutralized the toxicity activity of CdiA and was immunity protein as previous report. In conclusion, this is the first report that the functional CDI system is in probiotic EcN and might provide a potential competitive mechanism for probiotic EcN in intestinal microenvironment.