Farelli Jeremiah D, Galvin Brendan D, Li Zhiru, Liu Chunliang, Aono Miyuki, Garland Megan, Hallett Olivia E, Causey Thomas B, Ali-Reynolds Alana, Saltzberg Daniel J, Carlow Clotilde K S, Dunaway-Mariano Debra, Allen Karen N
Department of Chemistry, Boston University, Boston, Massachusetts, United States of America.
New England Biolabs, Division of Parasitology, Ipswich, Massachusetts, United States of America.
PLoS Pathog. 2014 Jul 3;10(7):e1004245. doi: 10.1371/journal.ppat.1004245. eCollection 2014 Jul.
Parasitic nematodes are responsible for devastating illnesses that plague many of the world's poorest populations indigenous to the tropical areas of developing nations. Among these diseases is lymphatic filariasis, a major cause of permanent and long-term disability. Proteins essential to nematodes that do not have mammalian counterparts represent targets for therapeutic inhibitor discovery. One promising target is trehalose-6-phosphate phosphatase (T6PP) from Brugia malayi. In the model nematode Caenorhabditis elegans, T6PP is essential for survival due to the toxic effect(s) of the accumulation of trehalose 6-phosphate. T6PP has also been shown to be essential in Mycobacterium tuberculosis. We determined the X-ray crystal structure of T6PP from B. malayi. The protein structure revealed a stabilizing N-terminal MIT-like domain and a catalytic C-terminal C2B-type HAD phosphatase fold. Structure-guided mutagenesis, combined with kinetic analyses using a designed competitive inhibitor, trehalose 6-sulfate, identified five residues important for binding and catalysis. This structure-function analysis along with computational mapping provided the basis for the proposed model of the T6PP-trehalose 6-phosphate complex. The model indicates a substrate-binding mode wherein shape complementarity and van der Waals interactions drive recognition. The mode of binding is in sharp contrast to the homolog sucrose-6-phosphate phosphatase where extensive hydrogen-bond interactions are made to the substrate. Together these results suggest that high-affinity inhibitors will be bi-dentate, taking advantage of substrate-like binding to the phosphoryl-binding pocket while simultaneously utilizing non-native binding to the trehalose pocket. The conservation of the key residues that enforce the shape of the substrate pocket in T6PP enzymes suggest that development of broad-range anthelmintic and antibacterial therapeutics employing this platform may be possible.
寄生线虫会引发严重疾病,困扰着发展中国家热带地区许多最贫困的人群。其中一种疾病是淋巴丝虫病,这是导致永久性和长期残疾的主要原因。线虫所必需但在哺乳动物中没有对应物的蛋白质是治疗性抑制剂发现的靶点。一个有前景的靶点是马来布鲁线虫的海藻糖-6-磷酸磷酸酶(T6PP)。在模式线虫秀丽隐杆线虫中,由于海藻糖6-磷酸积累的毒性作用,T6PP对生存至关重要。T6PP在结核分枝杆菌中也被证明是必不可少的。我们确定了马来布鲁线虫T6PP的X射线晶体结构。该蛋白质结构揭示了一个稳定的N端MIT样结构域和一个催化性的C端C2B型HAD磷酸酶折叠结构。结构导向诱变,结合使用设计的竞争性抑制剂海藻糖6-硫酸盐的动力学分析,确定了五个对结合和催化很重要的残基。这种结构-功能分析以及计算图谱为所提出的T6PP-海藻糖6-磷酸复合物模型提供了基础。该模型表明了一种底物结合模式,其中形状互补和范德华相互作用驱动识别。这种结合模式与同源的蔗糖-6-磷酸磷酸酶形成鲜明对比,后者与底物形成广泛的氢键相互作用。这些结果共同表明,高亲和力抑制剂将是双齿的,利用类似底物的结合方式结合到磷酸结合口袋,同时利用非天然结合方式结合到海藻糖口袋。T6PP酶中维持底物口袋形状的关键残基的保守性表明,利用这个平台开发广谱驱虫和抗菌治疗药物可能是可行的。