期刊
MICROBIOLOGY AND IMMUNOLOGY
卷 61, 期 6, 页码 206-214出版社
WILEY
DOI: 10.1111/1348-0421.12489
关键词
BopN; Bordetella; BteA; type III secretion system
资金
- MEXT/JSPS KAKENHI [24390108, 25670215, 26460535]
- Takeda Science Foundation
- Oyama Health Foundation
- Kitasato University Research Grant Program for Young Researchers
- Naito Foundation
- Grants-in-Aid for Scientific Research [24390108, 25670215, 17K08838, 16K08786] Funding Source: KAKEN
Bordetella bronchiseptica infects a wide variety of mammals, the type III secretion system (T3SS) being involved in long-term colonization by Bordetella of the trachea and lung. T3SS translocates virulence factors (commonly referred to as effectors) into host cells, leading to alterations in the host's physiological function. The Bordetella effectors BopN and BteA are known to have roles in up-regulation of IL-10 and cytotoxicity, respectively. Nevertheless, the mechanism by which BopN is translocated into host cells has not been examined in sufficient detail. Therefore, to determine the precise mechanisms of translocation of BopN into host cells, truncated derivatives of BopN were built and the derivatives' ability to translocate into host cells evaluated by adenylate cyclase-mediated translocation assay. It was found that N-terminal amino acid (aa) residues 1-200 of BopN are sufficient for its translocation into host cells. Interestingly, BopN translocation was completely blocked by deletion of the N-terminal aa residues 6-50, indicating that the N-terminal region is critical for BopN translocation. Furthermore, BopN appears to play an auxiliary role in BteA-mediated cytotoxicity. Thus, BopN can apparently translocate into host cells and may facilitate activity of BteA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据