首次于5年前在大腸桿菌中發(fā)現(xiàn)的“依賴于接觸的生長抑制” (CDI)，是“細(xì)胞到細(xì)胞接觸”用來抑制沒有這一體系的細(xì)菌細(xì)胞生長的一個(gè)機(jī)制,。CDI由“二伙伴”分泌蛋白CdiA 和 CdiB調(diào)控,，一個(gè)小的免疫蛋白CdiI保護(hù)其不受自身抑制作用影響。
現(xiàn)在CDI中所涉及的一些相互作用已經(jīng)搞清：CdiA的毒性被限制在該蛋白的羧基端(CdiA-CT),。對大腸桿菌其他菌種和細(xì)菌物種所做的搜索顯示這個(gè)體系是廣泛存在的,，一系列細(xì)菌含有一個(gè)或多個(gè)CdiA同源染色體，其中有不同的CdiA-CT毒素序列,。這些發(fā)現(xiàn)表明,，CDI體系構(gòu)成一個(gè)錯(cuò)綜復(fù)雜的免疫網(wǎng)絡(luò)，在環(huán)境中的細(xì)菌生長競爭中發(fā)揮一個(gè)重要功能,。（生物谷Bioon.com）
生物谷推薦英文摘要：
Nature doi:10.1038/nature09490
A widespread family of polymorphic contact-dependent toxin delivery systems in bacteria
Stephanie K. Aoki,Elie J. Diner,Claire t’Kint de Roodenbeke,Brandt R. Burgess,Stephen J. Poole,Bruce A. Braaten,Allison M. Jones,Julia S. Webb,Christopher S. Hayes,Peggy A. Cotter& David A. Low
Bacteria have developed mechanisms to communicate and compete with one another in diverse environments1. A new form of intercellular communication, contact-dependent growth inhibition (CDI), was discovered recently in Escherichia coli2. CDI is mediated by the CdiB/CdiA two-partner secretion (TPS) system. CdiB facilitates secretion of the CdiA ‘exoprotein’ onto the cell surface. An additional small immunity protein (CdiI) protects CDI+ cells from autoinhibition2, 3. The mechanisms by which CDI blocks cell growth and by which CdiI counteracts this growth arrest are unknown. Moreover, the existence of CDI activity in other bacteria has not been explored. Here we show that the CDI growth inhibitory activity resides within the carboxy-terminal region of CdiA (CdiA-CT), and that CdiI binds and inactivates cognate CdiA-CT, but not heterologous CdiA-CT. Bioinformatic and experimental analyses show that multiple bacterial species encode functional CDI systems with high sequence variability in the CdiA-CT and CdiI coding regions. CdiA-CT heterogeneity implies that a range of toxic activities are used during CDI. Indeed, CdiA-CTs from uropathogenic E.?coli and the plant pathogen Dickeya dadantii have different nuclease activities, each providing a distinct mechanism of growth inhibition. Finally, we show that bacteria lacking the CdiA-CT and CdiI coding regions are unable to compete with isogenic wild-type CDI+ cells both in laboratory media and on a eukaryotic host. Taken together, these results suggest that CDI systems constitute an intricate immunity network with an important function in bacterial competition.
