Rowe T, Kendrick-Jones J
MRC Laboratory of Molecular Biology, Cambridge, UK.
EMBO J. 1993 Dec;12(12):4877-84. doi: 10.1002/j.1460-2075.1993.tb06177.x.
In vertebrate smooth/non-muscle myosins, phosphorylation of the regulatory light chains by a specific calmodulin-activated kinase controls both myosin head interaction with actin and assembly of the myosin into filaments. Previous studies have shown that the C-terminal domain of the regulatory light chain is crucial for the regulation of these myosin functions. To further dissect the role of this region of the light chain in myosin regulation, a series of chicken smooth muscle myosin regulatory light chain mutants has been constructed with successive C-terminal deletions. These mutants were synthesized in Escherichia coli and analysed by their ability to restore Ca2+ regulation to scallop myosin that had been stripped of its native regulatory light chains ('desensitized'). The results show that regulatory light chain mutants with deletions in the C-terminal helix in subdomain 4 were able to reform the regulatory Ca2+ binding site on the scallop myosin head, but had lost the ability to suppress scallop myosin filament assembly and interaction with actin in the absence of Ca2+. Further deletions in the C-terminal domain led to a gradual loss of ability to restore the regulatory Ca2+ binding site. Thus, the regions in the C-terminal half of the regulatory light chain responsible for myosin regulation can be identified.
在脊椎动物的平滑肌/非肌肉肌球蛋白中,特定的钙调蛋白激活激酶对调节轻链的磷酸化作用,既能控制肌球蛋白头部与肌动蛋白的相互作用,也能控制肌球蛋白组装成细丝。先前的研究表明,调节轻链的C末端结构域对于这些肌球蛋白功能的调节至关重要。为了进一步剖析轻链这一区域在肌球蛋白调节中的作用,构建了一系列具有连续C末端缺失的鸡平滑肌肌球蛋白调节轻链突变体。这些突变体在大肠杆菌中合成,并通过它们恢复对已去除天然调节轻链(“脱敏”)的扇贝肌球蛋白的Ca2+调节能力进行分析。结果表明,在亚结构域4的C末端螺旋中有缺失的调节轻链突变体能够在扇贝肌球蛋白头部重新形成调节性Ca2+结合位点,但在没有Ca2+的情况下失去了抑制扇贝肌球蛋白细丝组装和与肌动蛋白相互作用的能力。C末端结构域的进一步缺失导致恢复调节性Ca2+结合位点的能力逐渐丧失。因此,可以确定调节轻链C末端一半中负责肌球蛋白调节的区域。