Department of Chemistry, Dartmouth College, 6128 Burke Laboratory, Hanover, NH 03755, USA.
Proc Natl Acad Sci U S A. 2010 Feb 16;107(7):2860-5. doi: 10.1073/pnas.0915021107. Epub 2010 Feb 1.
Cholera is an acute intestinal infection caused by the bacterium Vibrio cholerae. In order for V. cholerae to cause disease, it must produce two virulence factors, the toxin-coregulated pilus (TCP) and cholera toxin (CT), whose expression is controlled by a transcriptional cascade culminating with the expression of the AraC-family regulator, ToxT. We have solved the 1.9 A resolution crystal structure of ToxT, which reveals folds in the N- and C-terminal domains that share a number of features in common with AraC, MarA, and Rob as well as the unexpected presence of a buried 16-carbon fatty acid, cis-palmitoleate. The finding that cis-palmitoleic acid reduces TCP and CT expression in V. cholerae and prevents ToxT from binding to DNA in vitro provides a direct link between the host environment of V. cholerae and regulation of virulence gene expression.
霍乱是一种由霍乱弧菌引起的急性肠道感染。为了使霍乱弧菌引起疾病,它必须产生两种毒力因子,毒素调节菌毛(TCP)和霍乱毒素(CT),其表达受转录级联控制,最终表达 AraC 家族调节剂 ToxT。我们已经解决了 ToxT 的 1.9 A 分辨率晶体结构,该结构揭示了 N-和 C-末端结构域中的折叠,这些折叠与 AraC、MarA 和 Rob 具有许多共同特征,以及出人意料地存在一个埋藏的 16 碳脂肪酸,顺式棕榈油酸。发现在霍乱弧菌中,顺式棕榈油酸降低 TCP 和 CT 的表达,并防止 ToxT 在体外结合 DNA,这为霍乱弧菌的宿主环境与毒力基因表达调控之间提供了直接联系。