尽管中心体有助于在大多数细胞类型中组织纺锤体，但大多数物种的卵母细胞缺乏这些结构。在秀丽隐杆线虫卵母细胞的中心体纺锤体组装过程中，微管负端被向外分类远离形成极的染色体，但随后这些向外的力必须平衡以形成稳定的双极结构。同时，必须精确控制微管动力学以维持纺锤体长度和组织。人们对如何调整力和动力学以创建稳定的双极结构知之甚少。在这里，我们通过对 ZYG-8（一种保守的双皮质蛋白家族激酶）的研究，深入了解了这个问题；这种微管相关蛋白的哺乳动物同源物在许多癌症中表达上调，并且与细胞分裂有关，但其发挥作用的机制却知之甚少。我们发现卵母细胞中 ZYG-8 的消耗导致纺锤体过长，并伴有极和中纺锤体缺陷。重要的是，单极纺锤体实验表明，ZYG-8 耗尽会导致纺锤体内产生过多的向外力，并表明该蛋白质在调节产生力的马达 BMK-1/kinesin-5 方面具有潜在作用。此外，我们发现 ZYG-8 也是卵母细胞纺锤体内适当微管动力学所必需的，并且在减数分裂和有丝分裂期间其功能需要激酶活性。总而言之，我们的研究结果揭示了 ZYG-8 在卵母细胞中的新作用，并提供了关于如何稳定中心体纺锤体以促进忠实减数分裂的见解。版权所有：© 2024 Czajkowski 等人。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

Although centrosomes help organize spindles in most cell types, oocytes of most species lack these structures. During acentrosomal spindle assembly in C. elegans oocytes, microtubule minus ends are sorted outwards away from the chromosomes where they form poles, but then these outward forces must be balanced to form a stable bipolar structure. Simultaneously, microtubule dynamics must be precisely controlled to maintain spindle length and organization. How forces and dynamics are tuned to create a stable bipolar structure is poorly understood. Here, we have gained insight into this question through studies of ZYG-8, a conserved doublecortin-family kinase; the mammalian homolog of this microtubule-associated protein is upregulated in many cancers and has been implicated in cell division, but the mechanisms by which it functions are poorly understood. We found that ZYG-8 depletion from oocytes resulted in overelongated spindles with pole and midspindle defects. Importantly, experiments with monopolar spindles revealed that ZYG-8 depletion led to excess outward forces within the spindle and suggested a potential role for this protein in regulating the force-generating motor BMK-1/kinesin-5. Further, we found that ZYG-8 is also required for proper microtubule dynamics within the oocyte spindle and that kinase activity is required for its function during both meiosis and mitosis. Altogether, our findings reveal new roles for ZYG-8 in oocytes and provide insights into how acentrosomal spindles are stabilized to promote faithful meiosis.Copyright: © 2024 Czajkowski et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.