PDF(Pubmed)
Abstract：
KIFC3 is a member of Kinesin-14 family motor proteins, which play a variety of roles such as centrosome cohesion, cytokinesis, vesicles transportation and cell proliferation in mitosis. Here, we investigated the functional roles of KIFC3 in meiosis. Our findings demonstrated that KIFC3 exhibited expression and localization at centromeres during metaphase I, followed by translocation to the midbody at telophase I throughout mouse oocyte meiosis. Disruption of KIFC3 activity resulted in defective polar body extrusion. We observed aberrant meiotic spindles and misaligned chromosomes, accompanied by the loss of kinetochore-microtubule attachment, which might be due to the failed recruitment of BubR1/Bub3. Coimmunoprecipitation data revealed that KIFC3 plays a crucial role in maintaining the acetylated tubulin level mediated by Sirt2, thereby influencing microtubule stability. Additionally, our findings demonstrated an interaction between KIFC3 and PRC1 in regulating midbody formation during telophase I, which is involved in cytokinesis regulation. Collectively, these results underscore the essential contribution of KIFC3 to spindle assembly and cytokinesis during mouse oocyte meiosis.
摘要：
KIFC3是Kinesin-14家族运动蛋白的成员，它们扮演着各种角色，比如中心体凝聚力，胞质分裂,有丝分裂中的囊泡运输和细胞增殖。这里,我们研究了KIFC3在减数分裂中的功能作用。我们的发现表明，KIFC3在中期I中表现出在着丝粒的表达和定位，随后在整个小鼠卵母细胞减数分裂的末期I易位到中体。KIFC3活性的破坏导致极体挤出缺陷。我们观察到异常的减数分裂纺锤体和不对齐的染色体，伴随着动粒-微管附着的丧失，这可能是由于BubR1/Bub3的招聘失败。免疫共沉淀数据显示，KIFC3在维持Sirt2介导的乙酰化微管蛋白水平中起着至关重要的作用，从而影响微管的稳定性。此外,我们的研究结果表明，KIFC3和PRC1在调节终末期I的中体形成中存在相互作用，参与胞质分裂调节。总的来说，这些结果强调了KIFC3对小鼠卵母细胞减数分裂过程中纺锤体组装和胞质分裂的重要贡献.
