Hentschke Moritz, Trülzsch Konrad, Heesemann Jürgen, Aepfelbacher Martin, Ruckdeschel Klaus
Institute for Medical Microbiology, Virology and Hygiene, University Medical Center Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Infect Immun. 2007 Sep;75(9):4423-31. doi: 10.1128/IAI.00528-07. Epub 2007 Jul 2.
Pathogenic Yersinia spp. employ a type III protein secretion system that translocates several Yersinia outer proteins (Yops) into the host cell to modify the host immune response. One strategy of the infected host cell to resist the bacterial attack is degradation and inactivation of injected bacterial virulence proteins through the ubiquitin-proteasome pathway. The cytotoxin YopE is a known target protein of this major proteolytic system in eukaryotic cells. Here, we investigated the sensitivity of YopE belonging to different enteropathogenic Yersinia enterocolitica serogroups to ubiquitination and proteasomal degradation. Analysis of the YopE protein levels in proteasome inhibitor-treated versus untreated cells revealed that YopE from the highly pathogenic Y. enterocolitica serotype O8 was subjected to proteasomal destabilization, whereas the YopE isotypes from serogroups O3 and O9 evaded degradation. Accumulation of YopE from serotypes O3 and O9 was accompanied by an enhanced cytotoxic effect. Using Yersinia strains that specifically produced YopE from either Y. enterocolitica O8 or O9, we found that only the YopE protein from serogroup O8 was modified by polyubiquitination, although both YopE isotypes were highly homologous. We determined two unique N-terminal lysines (K62 and K75) in serogroup O8 YopE, not present in serogroup O9 YopE, that served as polyubiquitin acceptor sites. Insertion of either lysine in serotype O9 YopE enabled its ubiquitination and destabilization. These results define a serotype-dependent difference in the stability and activity of the Yersinia effector protein YopE that could influence Y. enterocolitica pathogenesis.
致病性耶尔森氏菌属利用III型蛋白分泌系统将几种耶尔森氏菌外蛋白(Yops)转运到宿主细胞中,以改变宿主免疫反应。受感染的宿主细胞抵抗细菌攻击的一种策略是通过泛素-蛋白酶体途径降解并使注入的细菌毒力蛋白失活。细胞毒素YopE是真核细胞中这种主要蛋白水解系统的已知靶蛋白。在此,我们研究了不同肠道致病性小肠结肠炎耶尔森氏菌血清群的YopE对泛素化和蛋白酶体降解的敏感性。分析蛋白酶体抑制剂处理的细胞与未处理的细胞中YopE蛋白水平,结果显示,高致病性小肠结肠炎耶尔森氏菌O8血清型的YopE会被蛋白酶体破坏稳定性,而O3和O9血清群的YopE同种型则逃避了降解。O3和O9血清型的YopE积累伴随着细胞毒性作用增强。使用特异性产生小肠结肠炎耶尔森氏菌O8或O9的YopE的耶尔森氏菌菌株,我们发现,尽管两种YopE同种型高度同源,但只有O8血清群的YopE蛋白被多聚泛素化修饰。我们在O8血清群YopE中确定了两个独特的N端赖氨酸(K62和K75),而O9血清群YopE中不存在这两个赖氨酸,它们作为多聚泛素受体位点。在O9血清型YopE中插入任一赖氨酸均可使其泛素化并破坏稳定性。这些结果确定了耶尔森氏菌效应蛋白YopE在稳定性和活性方面的血清型依赖性差异,这可能会影响小肠结肠炎耶尔森氏菌的发病机制。