Salmonella type III secretion-associated protein InvE controls translocation of effector proteins into host cells
Salmonella type III secretion-associated protein InvE controls translocation of effector proteins into host cells
复制标题
DOI：
10.1128/jb.184.17.4699-4708.2002
复制
发表时间：
2002-09-01
影响因子：
3.2
通讯作者：
Galán, JE
中科院分区：
文献类型：
--
作者：
Kubori, T;Galán, JE
肠炎沙门氏菌编码一个位于centiome 63(SPI-1)的致病岛上的III型分泌系统(TTSS)，这是其致病所必需的。该系统调节一组细菌蛋白进入宿主细胞，并具有调节细胞功能的能力。转移过程依赖于蛋白转位酶SipB、SIPC和SipD的功能。我们在这里报告了沙门氏菌蛋白INVe，它也在SPI-1中编码，对于细菌蛋白转移到宿主细胞是必不可少的。携带INVe功能缺失突变的一株鼠伤寒沙门氏菌突变体表现出SipB、SIPC和SipD的分泌减少，而其他TTSS效应蛋白的分泌增加。我们还证明了INVe与SipB、SIPC及其同源伴侣SICA形成的蛋白质复合体相互作用。我们认为INVe通过调节sip蛋白转位酶的功能来控制蛋白质的转位。
Salmonella enterica encodes a type III secretion system (TTSS) within a pathogenicity island located at centisome 63 (SPI-1), which is essential for its pathogenicity. This system mediates the transfer of a battery of bacterial proteins into the host cell with the capacity to modulate cellular functions. The transfer process is dependent on the function of protein translocases SipB, SipC, and SipD. We report here that Salmonella protein InvE, which is also encoded within SPI-1, is essential for the translocation of bacterial proteins into host cells. An S. enterica serovar Typhimurium mutant carrying a loss-of-function mutation in invE shows reduced secretion of SipB, SipC, and SipD while exhibiting increased secretion of other TTSS effector proteins. We also demonstrate that InvE interacts with a protein complex formed by SipB, SipC, and their cognate chaperone, SicA. We propose that InvE controls protein translocation by regulating the function of the Sip protein translocases.