Hu Haitao, Chazin Walter J
Departments of Biochemistry and Physics, Center for Structural Biology, Vanderbilt University, 5142 BIOSCI/MRBIII, Nashville, TN 37232-8725, USA.
J Mol Biol. 2003 Jul 11;330(3):473-84. doi: 10.1016/s0022-2836(03)00619-3.
Caltractin (centrin) is a member of the calmodulin (CaM) superfamily of EF-hand calcium-binding proteins. It is an essential component of the centrosomal structures in a wide range of organisms. Caltractin and calmodulin apparently function in distinct calcium signaling pathways despite substantial sequence similarity. In an effort to understand the structural basis for such differences, the high-resolution three-dimensional solution structure of the complex between the Ca(2+)-activated C-terminal domain of Chlamydomonas reinhardtii caltractin (CRC-C) and a 19 residue peptide fragment comprising the putative cdc31p-binding region of Kar1p (K(19)) has been determined by multi-dimensional heteronuclear NMR spectroscopy. Formation of the complex is calcium-dependent and is stabilized by extensive interactions between CRC-C and three key hydrophobic anchors (Trp10, Leu13 and Leu14) in the peptide as well as favorable electrostatic interactions at the protein-peptide interface. In-depth comparisons have been made to the structure of the complex of Ca(2+)-activated calmodulin and R(20), the CaM-binding domain of smooth muscle myosin light-chain kinase. Although the overall structures of CRC and CaM domains in their respective complexes are very similar, differences in critical regions in the sequences of these proteins and their targets lead to clear differences in the complementarity of their respective binding surfaces. These subtle differences reveal the structural basis for the Ca(2+)-dependent regulation of distinct cellular signaling events by CRC and CaM.
钙牵蛋白(中心蛋白)是EF手型钙结合蛋白钙调蛋白(CaM)超家族的成员。它是多种生物体中心体结构的重要组成部分。尽管序列相似度很高,但钙牵蛋白和钙调蛋白显然在不同的钙信号通路中发挥作用。为了理解这种差异的结构基础,通过多维异核核磁共振光谱法确定了莱茵衣藻钙牵蛋白(CRC-C)的Ca(2+)激活C末端结构域与包含Kar1p假定的cdc31p结合区域的19个残基肽片段(K(19))之间复合物的高分辨率三维溶液结构。复合物的形成依赖于钙,并通过CRC-C与肽中的三个关键疏水锚定残基(Trp10、Leu13和Leu14)之间的广泛相互作用以及蛋白质-肽界面处有利的静电相互作用而稳定。已对Ca(2+)激活的钙调蛋白与平滑肌肌球蛋白轻链激酶的CaM结合结构域R(20)的复合物结构进行了深入比较。尽管CRC和CaM结构域在各自复合物中的整体结构非常相似,但这些蛋白质及其靶标序列中关键区域的差异导致它们各自结合表面的互补性存在明显差异。这些细微差异揭示了CRC和CaM对不同细胞信号事件进行Ca(2+)依赖性调节的结构基础。