1] Departments of Molecular Biology and Biochemistry, Chemistry, and Pharmaceutical Sciences, University of California, Irvine, California 92697, USA [2].
1] Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California 92093, USA [2].
Nature. 2014 Jan 16;505(7483):427-31. doi: 10.1038/nature12810. Epub 2013 Dec 22.
Acyl carrier protein (ACP) transports the growing fatty acid chain between enzymatic domains of fatty acid synthase (FAS) during biosynthesis. Because FAS enzymes operate on ACP-bound acyl groups, ACP must stabilize and transport the growing lipid chain. ACPs have a central role in transporting starting materials and intermediates throughout the fatty acid biosynthetic pathway. The transient nature of ACP-enzyme interactions impose major obstacles to obtaining high-resolution structural information about fatty acid biosynthesis, and a new strategy is required to study protein-protein interactions effectively. Here we describe the application of a mechanism-based probe that allows active site-selective covalent crosslinking of AcpP to FabA, the Escherichia coli ACP and fatty acid 3-hydroxyacyl-ACP dehydratase, respectively. We report the 1.9 Å crystal structure of the crosslinked AcpP-FabA complex as a homodimer in which AcpP exhibits two different conformations, representing probable snapshots of ACP in action: the 4'-phosphopantetheine group of AcpP first binds an arginine-rich groove of FabA, then an AcpP helical conformational change locks AcpP and FabA in place. Residues at the interface of AcpP and FabA are identified and validated by solution nuclear magnetic resonance techniques, including chemical shift perturbations and residual dipolar coupling measurements. These not only support our interpretation of the crystal structures but also provide an animated view of ACP in action during fatty acid dehydration. These techniques, in combination with molecular dynamics simulations, show for the first time that FabA extrudes the sequestered acyl chain from the ACP binding pocket before dehydration by repositioning helix III. Extensive sequence conservation among carrier proteins suggests that the mechanistic insights gleaned from our studies may be broadly applicable to fatty acid, polyketide and non-ribosomal biosynthesis. Here the foundation is laid for defining the dynamic action of carrier-protein activity in primary and secondary metabolism, providing insight into pathways that can have major roles in the treatment of cancer, obesity and infectious disease.
酰基载体蛋白 (ACP) 在脂肪酸合成过程中,于脂肪酸合酶 (FAS) 的酶结构域之间转运不断增长的脂肪酸链。由于 FAS 酶作用于 ACP 结合的酰基,因此 ACP 必须稳定并转运不断增长的脂质链。ACP 在脂肪酸生物合成途径中转运起始材料和中间产物方面发挥着核心作用。ACP-酶相互作用的瞬时性质对获得关于脂肪酸生物合成的高分辨率结构信息造成了重大障碍,因此需要一种新的策略来有效地研究蛋白质-蛋白质相互作用。在这里,我们描述了一种基于机制的探针的应用,该探针可使 AcpP 与 FabA(大肠杆菌 ACP 和脂肪酸 3-羟基酰基-ACP 脱水酶)分别发生活性位点选择性的共价交联。我们报告了交联的 AcpP-FabA 复合物的 1.9 Å 晶体结构,其为同源二聚体,其中 AcpP 呈现两种不同的构象,代表 ACP 作用中的可能瞬时状态:AcpP 的 4′-磷酸泛酰巯基乙胺基团首先与 FabA 的富含精氨酸的凹槽结合,然后 AcpP 的构象变化使 AcpP 和 FabA 锁定在适当的位置。通过溶液核磁共振技术,包括化学位移扰动和残余偶极耦合测量,鉴定和验证了 AcpP 和 FabA 界面的残基。这些不仅支持我们对晶体结构的解释,而且还提供了脂肪酸脱水过程中 ACP 作用的动画视图。这些技术与分子动力学模拟相结合,首次表明 FabA 通过重新定位 III 螺旋将封闭的酰基链从 ACP 结合口袋中挤出,然后进行脱水。载体蛋白之间广泛的序列保守性表明,从我们的研究中获得的机制见解可能广泛适用于脂肪酸、聚酮和非核糖体生物合成。在这里,为定义载体蛋白活性在初级和次级代谢中的动态作用奠定了基础,为了解在癌症、肥胖和传染病的治疗中可能具有重要作用的途径提供了深入的见解。