PDF(Pubmed)
Abstract：
During C. elegans oocyte meiosis I cytokinesis and polar body extrusion, cortical actomyosin is locally remodeled to assemble a contractile ring that forms within and remains part of a much larger and actively contractile cortical actomyosin network. This network both mediates contractile ring dynamics and generates shallow ingressions throughout the oocyte cortex during polar body extrusion. Based on our analysis of requirements for CLS-2, a member of the CLASP family of proteins that stabilize microtubules, we recently proposed that a balance of actomyosin-mediated tension and microtubule-mediated stiffness limits membrane ingression throughout the oocyte during meiosis I polar body extrusion. Here, using live cell imaging and fluorescent protein fusions, we show that CLS-2 is part of a group of kinetochore proteins, including the scaffold KNL-1 and the kinase BUB-1, that also co-localize during meiosis I to structures called linear elements, which are present within the assembling oocyte spindle and also are distributed throughout the oocyte in proximity to, but appearing to underlie, the actomyosin cortex. We further show that KNL-1 and BUB-1, like CLS-2, promote the proper organization of sub-cortical microtubules and also limit membrane ingression throughout the oocyte. Moreover, nocodazole or taxol treatment to destabilize or stabilize oocyte microtubules leads to, respectively, excess or decreased membrane ingression throughout the oocyte. Furthermore, taxol treatment, and genetic backgrounds that elevate the levels of cortically associated microtubules, both suppress excess membrane ingression in cls-2 mutant oocytes. We propose that linear elements influence the organization of sub-cortical microtubules to generate a stiffness that limits cortical actomyosin-driven membrane ingression throughout the oocyte during meiosis I polar body extrusion. We discuss the possibility that this regulation of sub-cortical microtubule dynamics facilitates actomyosin contractile ring dynamics during C. elegans oocyte meiosis I cell division.
摘要：
在秀丽隐杆线虫卵母细胞减数分裂和极体挤压期间，皮质肌动球蛋白被局部重塑以组装收缩环，该收缩环在内部形成并保留为更大且活跃收缩的皮质肌动球蛋白网络的一部分。该网络既介导收缩环动力学，又在极体挤压过程中在整个卵母细胞皮层中产生浅层沉积。根据我们对CLS-2的需求分析，CLASP家族中稳定微管的蛋白质，我们最近提出，肌动球蛋白介导的张力和微管介导的刚度的平衡限制了减数分裂I极体挤压过程中整个卵母细胞的膜侵入。这里,使用活细胞成像和荧光蛋白融合，我们证明CLS-2是一组动粒蛋白的一部分，包括支架KNL-1和激酶BUB-1，它们在减数分裂I期间也共同定位到称为线性元件的结构，它们存在于组装的卵母细胞纺锤体中，也分布在整个卵母细胞附近，但似乎是底层的，肌动球蛋白皮质.我们进一步表明，KNL-1和BUB-1与CLS-2一样，可促进皮质下微管的适当组织，并限制整个卵母细胞的膜侵入。此外，诺考达唑或紫杉醇治疗使卵母细胞微管不稳定或稳定，分别,整个卵母细胞的膜侵入过量或减少。此外，紫杉醇治疗，和遗传背景提高了皮质相关微管的水平，两者都能抑制cls-2突变卵母细胞的过度膜侵入。我们建议线性元件影响皮质下微管的组织，以产生刚度，从而限制减数分裂I极体挤压过程中皮质肌动球蛋白驱动的膜进入整个卵母细胞。我们讨论了在秀丽隐杆线虫卵母细胞减数分裂I细胞分裂过程中，皮质下微管动力学的这种调节促进肌动球蛋白收缩环动力学的可能性。
