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A Global Myosin Light Chain Kinase-dependent Increase in Myosin II Contractility Accompanies the Metaphase–Anaphase Transition in Sea Urchin Eggs

机译:全球肌球蛋白II收缩力的肌球蛋白轻链激酶依赖性增加伴随着海胆卵的中期到后期过渡。

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摘要

Myosin II is the force-generating motor for cytokinesis, and although it is accepted that myosin contractility is greatest at the cell equator, the temporal and spatial cues that direct equatorial contractility are not known. Dividing sea urchin eggs were placed under compression to study myosin II-based contractile dynamics, and cells manipulated in this manner underwent an abrupt, global increase in cortical contractility concomitant with the metaphase–anaphase transition, followed by a brief relaxation and the onset of furrowing. Prefurrow cortical contractility both preceded and was independent of astral microtubule elongation, suggesting that the initial activation of myosin II preceded cleavage plane specification. The initial rise in contractility required myosin light chain kinase but not Rho-kinase, but both signaling pathways were required for successful cytokinesis. Last, mobilization of intracellular calcium during metaphase induced a contractile response, suggesting that calcium transients may be partially responsible for the timing of this initial contractile event. Together, these findings suggest that myosin II-based contractility is initiated at the metaphase–anaphase transition by Ca2+-dependent myosin light chain kinase (MLCK) activity and is maintained through cytokinesis by both MLCK- and Rho-dependent signaling. Moreover, the signals that initiate myosin II contractility respond to specific cell cycle transitions independently of the microtubule-dependent cleavage stimulus.
机译:肌球蛋白II是胞质分裂的力产生马达,尽管人们公认肌球蛋白的收缩力在细胞赤道处最大,但指导赤道收缩力的时间和空间线索尚不清楚。将分开的海胆卵置于压缩状态下研究基于肌球蛋白II的收缩动力学,以这种方式操作的细胞伴随着中期到后期的转变而突然突然,整体地增加了皮质的收缩力,随后短暂地放松并开始犁沟。犁沟前的皮质收缩力先于并独立于星形微管伸长,这表明肌球蛋白II的初始活化先于分裂平面。收缩力的最初升高需要肌球蛋白轻链激酶,而不是Rho激酶,但是成功的胞质分裂需要两条信号通路。最后,细胞中期钙的动员在中期引起了收缩反应,这表明钙瞬变可能部分负责这一初始收缩事件的发生时间。在一起,这些发现表明基于肌球蛋白II的收缩力是在中期到后期通过Ca 2 + 依赖的肌球蛋白轻链激酶(MLCK)活性而启动的,并且通过MLCK-和Rho依赖性信号传导。此外,启动肌球蛋白II收缩力的信号独立于微管依赖的裂解刺激响应特定的细胞周期转换。

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