Bobkov A A, Bobkova E A, Lin S H, Reisler E
Department of Chemistry and Biochemistry and the Molecular Biology Institute, School of Medicine, Center for Health Sciences, University of California, Los Angeles 90095, USA.
Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2285-9. doi: 10.1073/pnas.93.6.2285.
A characteristic feature of all myosins is the presence of two sequences which despite considerable variations in length and composition can be aligned with loops 1 (residues 204-216) and 2 (residues 627-646) in the chicken myosin-head heavy chain sequence. Recently, an intriguing hypothesis has been put forth suggesting that diverse performances of myosin motors are achieved through variations in the sequences of loops 1 and 2 [Spudich, J. (1994) Nature (London) 372, 515-518]. Here, we report on the study of the effects of tryptic digestion of these loops on the motor and enzymatic functions of myosin. Tryptic digestions of myosin, which produced heavy meromyosin (HMM) with different percentages of molecules cleaved at both loop 1 and loop 2, resulted in the consistent decrease in the sliding velocity of actin filaments over HMM in the in vitro motility assays, did not affect the Vmax, and increased the Km values for actin-activated ATPase of HMM. Selective cleavage of loop 2 on HMM decreased its affinity for actin but did not change the sliding velocity of actin in the in vitro motility assays. The cleavage of loop 1 and HMM decreased the mean sliding velocity of actin in such assays by almost 50% but did not alter its affinity for HMM. To test for a possible kinetic determinant of the change in motility, 1-N6-ethenoadenosine diphosphate (epsilon-ADP) release from cleaved and uncleaved myosin subfragment 1 (S1) was examined. Tryptic digestion of loop 1 slightly accelerated the release of epsilon-ADP from S1 but did not affect the rate of epsilon-ADP release from acto-S1 complex. Overall, the results of this work support the hypothesis that loop 1 can modulate the motor function of myosin and suggest that such modulation involves a mechanism other than regulation of ADP release from myosin.
所有肌球蛋白的一个特征是存在两个序列,尽管其长度和组成有很大差异,但可与鸡肌球蛋白头部重链序列中的环1(第204 - 216位氨基酸残基)和环2(第627 - 646位氨基酸残基)比对。最近,有人提出了一个有趣的假说,认为肌球蛋白马达的不同性能是通过环1和环2序列的变化实现的[斯普迪奇,J.(1994年)《自然》(伦敦)372, 515 - 518]。在此,我们报告了对这些环的胰蛋白酶消化对肌球蛋白的马达和酶功能影响的研究。对肌球蛋白进行胰蛋白酶消化,产生了重酶解肌球蛋白(HMM),其中不同百分比的分子在环1和环2处均被切割,在体外运动测定中,这导致肌动蛋白丝在HMM上的滑动速度持续下降,不影响最大反应速度(Vmax),并增加了HMM的肌动蛋白激活ATP酶的米氏常数(Km值)。对HMM上的环2进行选择性切割降低了其对肌动蛋白的亲和力,但在体外运动测定中未改变肌动蛋白的滑动速度。对环1和HMM进行切割使此类测定中肌动蛋白的平均滑动速度降低了近50%,但未改变其对HMM的亲和力。为了测试运动变化的可能动力学决定因素,检测了切割和未切割的肌球蛋白亚片段1(S1)中1 - N6 - 乙烯基腺苷二磷酸(ε - ADP)的释放。对环1进行胰蛋白酶消化略微加速了ε - ADP从S1的释放,但不影响ε - ADP从肌动蛋白 - S1复合物的释放速率。总体而言,这项工作的结果支持环1可调节肌球蛋白马达功能的假说,并表明这种调节涉及一种不同于调节肌球蛋白释放ADP的机制。