Pyburn Tasia M, Foegeding Nora J, González-Rivera Christian, McDonald Nathan A, Gould Kathleen L, Cover Timothy L, Ohi Melanie D
Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, 37232.
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN, 37232.
Mol Microbiol. 2016 Oct;102(1):22-36. doi: 10.1111/mmi.13443. Epub 2016 Jul 8.
Helicobacter pylori colonizes the human stomach and is a potential cause of peptic ulceration or gastric adenocarcinoma. H. pylori secretes a pore-forming toxin known as vacuolating cytotoxin A (VacA). The 88 kDa secreted VacA protein, composed of an N-terminal p33 domain and a C-terminal p55 domain, assembles into water-soluble oligomers. The structural organization of membrane-bound VacA has not been characterized in any detail and the role(s) of specific VacA domains in membrane binding and insertion are unclear. We show that membrane-bound VacA organizes into hexameric oligomers. Comparison of the two-dimensional averages of membrane-bound and soluble VacA hexamers generated using single particle electron microscopy reveals a structural difference in the central region of the oligomers (corresponding to the p33 domain), suggesting that membrane association triggers a structural change in the p33 domain. Analyses of the isolated p55 domain and VacA variants demonstrate that while the p55 domain can bind membranes, the p33 domain is required for membrane insertion. Surprisingly, neither VacA oligomerization nor the presence of putative transmembrane GXXXG repeats in the p33 domain is required for membrane insertion. These findings provide new insights into the process by which VacA binds and inserts into the lipid bilayer to form membrane channels.
幽门螺杆菌定殖于人的胃部,是消化性溃疡或胃腺癌的潜在病因。幽门螺杆菌分泌一种名为空泡毒素A(VacA)的成孔毒素。分泌的88 kDa VacA蛋白由N端的p33结构域和C端的p55结构域组成,可组装成水溶性寡聚体。膜结合型VacA的结构组织尚未得到详细表征,特定VacA结构域在膜结合和插入中的作用尚不清楚。我们发现膜结合型VacA组装成六聚体寡聚体。使用单颗粒电子显微镜对膜结合型和可溶性VacA六聚体的二维平均值进行比较,揭示了寡聚体中心区域(对应于p33结构域)的结构差异,表明膜结合会触发p33结构域的结构变化。对分离的p55结构域和VacA变体的分析表明,虽然p55结构域可以结合膜,但膜插入需要p33结构域。令人惊讶的是,膜插入既不需要VacA寡聚化,也不需要p33结构域中假定的跨膜GXXXG重复序列的存在。这些发现为VacA结合并插入脂质双层以形成膜通道的过程提供了新的见解。