Kar Alak Kanti, Roy Polly
Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
J Virol. 2003 Nov;77(21):11347-56. doi: 10.1128/jvi.77.21.11347-11356.2003.
The VP6 protein of bluetongue virus possesses a number of activities, including nucleoside triphosphatase, RNA binding, and helicase activity (N. Stauber, J. Martinez-Costas, G. Sutton, K. Monastyrskaya, and P. Roy, J. Virol. 71:7220-7226, 1997). Although the enzymatic functions of the protein have been documented, a detailed structure and function study has not been completed and the oligomeric form of the protein in solution has not been described. In this study, we have characterized VP6 activity by creating site-directed mutations in the putative functional helicase domains. Mutant proteins were expressed at high levels in an insect cell by using recombinant baculoviruses purified and analyzed for ATP binding, ATP hydrolysis, and RNA unwinding activities. UV cross-linking experiments indicated that the lysine residue in the conserved motif AXXGXGK(110)V is directly involved in ATP binding, whereas mutant R(205)Q in the arginine-rich motif ER(205)XGRXXR bound ATP at a level comparable to that of the wild-type protein. The RNA binding activity was drastically altered in the R(205)Q mutant and was also affected in the K(110)N mutant. Helicase activity was altered in both mutants. The mutation E(157)N in the DEXX sequence, presumed to act as a Walker B motif, showed an intermediate activity, implying that this motif does not play a crucial role in VP6 function. Purified protein demonstrated stable oligomers with a ring-like morphology in the presence of nucleic acids similar to those shown by other helicases. Gel filtration chromatography, native gel electrophoresis, and glycerol gradient analysis clearly indicated multiple oligomeric forms of VP6.
蓝舌病病毒的VP6蛋白具有多种活性,包括核苷三磷酸酶、RNA结合和解旋酶活性(N. 施陶伯、J. 马丁内斯 - 科斯塔斯、G. 萨顿、K. 莫纳斯蒂尔斯卡娅和P. 罗伊,《病毒学杂志》71:7220 - 7226,1997年)。尽管该蛋白的酶促功能已有文献记载,但尚未完成详细的结构与功能研究,且溶液中该蛋白的寡聚形式也未被描述。在本研究中,我们通过在假定的功能性解旋酶结构域中创建定点突变来表征VP6活性。利用重组杆状病毒在昆虫细胞中高水平表达突变蛋白,对其进行纯化并分析ATP结合、ATP水解和RNA解旋活性。紫外线交联实验表明,保守基序AXXGXGK(110)V中的赖氨酸残基直接参与ATP结合,而富含精氨酸基序ER(205)XGRXXR中的突变体R(205)Q结合ATP的水平与野生型蛋白相当。R(205)Q突变体的RNA结合活性发生了显著改变,K(110)N突变体的RNA结合活性也受到了影响。两个突变体的解旋酶活性均发生了改变。推测作为沃克B基序起作用的DEXX序列中的突变E(157)N表现出中等活性,这意味着该基序在VP6功能中并不起关键作用。纯化的蛋白在存在核酸的情况下显示出具有环状形态的稳定寡聚体,类似于其他解旋酶所显示的那样。凝胶过滤色谱、非变性凝胶电泳和甘油梯度分析清楚地表明了VP6的多种寡聚形式。