Mortishire-Smith R J, Pitzenberger S M, Burke C J, Middaugh C R, Garsky V M, Johnson R G
Neuroscience Research Centre, Merck Sharp and Dohme Research Laboratories, Harlow, Essex, United Kingdom.
Biochemistry. 1995 Jun 13;34(23):7603-13. doi: 10.1021/bi00023a006.
Peptides representing the N-terminal domain (Ia) of the cardiac sarcoplasmic reticulum protein phospholamban (residues 1-25 [PLB(1-25)] and a phosphorylated form [pPLB(1-25)]) were synthesized and their conformations examined using circular dichroism and nuclear magnetic resonance spectroscopy. In aqueous solution, both PLB(1-25) and pPLB(1-25) adopt a primarily disordered conformation. In 30% trifluoroethanol/10 mM phosphate, PLB(1-25) exhibits a CD spectrum consistent with 60% helical structure. This value decreases to 27% for the phosphorylated peptide. CD spectra in 2% SDS indicate 40% alpha-helix for PLB(1-25) and 20% for pPLB(1-25). Full chemical shift assignments were obtained by conventional homonuclear NMR methodologies for both PLB(1-25) and pPLB(1-25) in 30% trifluoroethanol/water and 300 mM SDS. The solution structure of PLB(1-25) in 30% TFE/water was determined from distance geometry calculations using 54 NOE distance constraints and 17 torsion angle constraints. In the family of 20 calculated conformers, the root mean square deviation from the mean structure is 0.79 A for backbone heavy atoms of residues 1-17. The structure comprises a regular alpha-helix extending from M1 to S16 with the remaining C-terminal residues disordered. The calculated structure is supported by analysis of C alpha H secondary shifts which are significantly negative for residues 1-16. Chemical shift degeneracy is substantially more extensive in the phospho form and precludes a direct comparison of calculated structures. However, the magnitudes of upfield secondary shifts are decreased by 20% in residues 1-11 and are not significantly helical for residues 12-16 according to the criteria of Wishart et al. [(1992) Biochemistry 31, 1647-1651]. 3JHN alpha coupling constants measured for I12, R13, A15, and S16 also suggest that residues 12-16 undergo a local unwinding of the helix upon phosphorylation. Similar results are obtained for PLB(1-25) and pPLB(1-25) in 300 mM perdeuterated sodium dodecyl sulfate except that differences in backbone dynamics for the helical and nonhelical regions of the peptide are evident in the DQF-COSY line shapes for fingerprint cross-peaks. This disruption of structure at the C-terminus of the helix suggests a model for phosphorylation-induced dissociation of the PLB/Ca(2+)-ATPase complex.
合成了代表心肌肌浆网蛋白受磷蛋白N端结构域(Ia)的肽段(残基1 - 25 [PLB(1 - 25)]及其磷酸化形式[pPLB(1 - 25)]),并使用圆二色光谱和核磁共振光谱研究了它们的构象。在水溶液中,PLB(1 - 25)和pPLB(1 - 25)主要呈无序构象。在30%三氟乙醇/10 mM磷酸盐中,PLB(1 - 25)的圆二色光谱表明其具有60%的螺旋结构。对于磷酸化肽段,该值降至27%。在2%十二烷基硫酸钠中的圆二色光谱表明PLB(1 - 25)有40%的α - 螺旋,pPLB(1 - 25)有20%的α - 螺旋。通过常规的同核核磁共振方法,在30%三氟乙醇/水和300 mM十二烷基硫酸钠中获得了PLB(1 - 25)和pPLB(1 - 25)的完整化学位移归属。利用54个核Overhauser效应(NOE)距离约束和17个扭转角约束,通过距离几何计算确定了PLB(1 - 25)在30%三氟乙醇/水中的溶液结构。在20个计算构象的家族中,残基1 - 17主链重原子与平均结构的均方根偏差为0.79 Å。该结构包含一个从M1延伸至S16的规则α - 螺旋,其余C端残基无序。对CαH二级位移的分析支持了计算结构,残基1 - 16的二级位移显著为负。在磷酸化形式中,化学位移简并更为广泛,排除了对计算结构进行直接比较的可能性。然而,根据Wishart等人[(1992) Biochemistry 31, 1647 - 1651]的标准,残基1 - 11的上场二级位移幅度降低了20%,残基12 - 16的螺旋性不显著。对I12、R13、A15和S16测量的3JHNα耦合常数也表明,磷酸化后残基12 - 16的螺旋发生局部解旋。在300 mM全氘代十二烷基硫酸钠中,PLB(1 - 25)和pPLB(1 - 25)也得到了类似结果,只是肽段螺旋和非螺旋区域主链动力学的差异在指纹交叉峰的双量子滤波相关谱(DQF - COSY)线形中很明显。螺旋C端结构的这种破坏提示了一种磷蛋白/钙(2 +)-ATP酶复合物磷酸化诱导解离的模型。