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CDK-1 inhibits meiotic spindle shortening and dynein-dependent spindle rotation in C. elegans

机译:CDK-1抑制线虫的减数分裂纺锤体缩短和动力蛋白依赖性纺锤体旋转

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摘要

In animals, the female meiotic spindle is positioned at the egg cortex in a perpendicular orientation to facilitate the disposal of half of the chromosomes into a polar body. In Caenorhabditis elegans, the metaphase spindle lies parallel to the cortex, dynein is dispersed on the spindle, and the dynein activators ASPM-1 and LIN-5 are concentrated at spindle poles. Anaphase-promoting complex (APC) activation results in dynein accumulation at spindle poles and dynein-dependent rotation of one spindle pole to the cortex, resulting in perpendicular orientation. To test whether the APC initiates spindle rotation through cyclin B–CDK-1 inactivation, separase activation, or degradation of an unknown dynein inhibitor, CDK-1 was inhibited with purvalanol A in metaphase-I–arrested, APC-depleted embryos. CDK-1 inhibition resulted in the accumulation of dynein at spindle poles and dynein-dependent spindle rotation without chromosome separation. These results suggest that CDK-1 blocks rotation by inhibiting dynein association with microtubules and with LIN-5–ASPM-1 at meiotic spindle poles and that the APC promotes spindle rotation by inhibiting CDK-1.
机译:在动物中,雌性减数分裂纺锤体以垂直方向位于卵皮层,以便于将一半的染色体处理到极体中。在秀丽隐杆线虫中,中期纺锤体平行于皮质,动力蛋白分散在纺锤体上,动力蛋白激活剂ASPM-1和LIN-5集中在纺锤极。后期促进复合物(APC)激活导致动力蛋白在纺锤极上积聚,并导致一个纺锤极向皮层的依赖于动力蛋白的旋转,从而导致垂直方向。为了测试APC是否通过细胞周期蛋白B–CDK-1失活,分离酶激活或未知的动力蛋白抑制剂的降解来启动纺锤体旋转,在戊烷醇A抑制的I期中期,APC耗尽的胚胎中,CDK-1被嘌呤醇A抑制。 CDK-1的抑制导致动力蛋白在纺锤极上的积累和依赖动力蛋白的纺锤旋转,而没有染色体分离。这些结果表明,CDK-1通过抑制动力蛋白与微管和减数分裂纺锤体极上的LIN-5-ASPM-1缔合而阻止旋转,而APC通过抑制CDK-1促进纺锤体旋转。

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