A cdk1 gradient guides surface contraction waves in oocytes.

A cdk1 gradient guides surface contraction waves in oocytes.
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DOI:
10.1038/s41467-017-00979-6
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发表时间:
2017-10-11
影响因子:
16.6
通讯作者:
Lénárt P
Lénárt P
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Bischof J;Brand CA;Somogyi K;Májer I;Thome S;Mori M;Schwarz US;Lénárt P

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卵母细胞和胚胎中的表面收缩波(SCW)导致与细胞周期转换耦合的大规模形状变化,并且在空间上与细胞轴协调。在这里,我们表明,超临界水在海星卵母细胞所产生的肌球蛋白II驱动的皮质收缩的旅行带。在带的前部,收缩性通过去除RhoA/RhoA激酶/肌球蛋白II信号传导模块的cdk 1抑制而被激活,而在后部,收缩性通过源自RhoA激酶下游的负反馈而被关闭。SCW的方向性和速度由cdk 1-cyclinB的时空梯度控制。这种梯度是由cdk 1-cyclinB从不对称定位的细胞核释放和cyclinB的进行性降解形成的。通过结合定量成像,生化和机械扰动与数学建模,我们证明了SCW的结果从时空整合的两个保守的调控模块,cdk 1-cyclinB细胞周期调控和RhoA/Rok/NMYII肌动球蛋白收缩。表面收缩波(SCW)是卵母细胞中与细胞周期转换相关的显著形状变化。在这里,作者表明,SCW是由两个保守的模块,cdk 1-cyclinB的细胞周期调控和RhoA/Rok/NMYII的肌动球蛋白收缩性的时空整合模式。
Surface contraction waves (SCWs) in oocytes and embryos lead to large-scale shape changes coupled to cell cycle transitions and are spatially coordinated with the cell axis. Here, we show that SCWs in the starfish oocyte are generated by a traveling band of myosin II-driven cortical contractility. At the front of the band, contractility is activated by removal of cdk1 inhibition of the RhoA/RhoA kinase/myosin II signaling module, while at the rear, contractility is switched off by negative feedback originating downstream of RhoA kinase. The SCW’s directionality and speed are controlled by a spatiotemporal gradient of cdk1-cyclinB. This gradient is formed by the release of cdk1-cyclinB from the asymmetrically located nucleus, and progressive degradation of cyclinB. By combining quantitative imaging, biochemical and mechanical perturbations with mathematical modeling, we demonstrate that the SCWs result from the spatiotemporal integration of two conserved regulatory modules, cdk1-cyclinB for cell cycle regulation and RhoA/Rok/NMYII for actomyosin contractility. Surface contraction waves (SCWs) are prominent shape changes coupled to cell cycle transitions in oocytes. Here the authors show that SCWs are patterned by the spatiotemporal integration of two conserved modules, cdk1-cyclinB for cell cycle regulation and RhoA/Rok/NMYII for actomyosin contractility.
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