Manandhar G, Moreno R D, Simerly C, Toshimori K, Schatten G
Departments of Obstetrics & Gynecology and Cell & Developmental Biology, Oregon Regional Primate Research Center, Oregon Health Sciences University, Beaverton, OR 97006, USA.
J Cell Sci. 2000 Dec;113 Pt 23:4275-86. doi: 10.1242/jcs.113.23.4275.
Mouse male meiotic cytokinesis was studied using immunofluorescent probes against various elements of cytokinetic apparatus and electron microscopy. In normal mice, some spermatocytes fail to undergo cytokinesis after meiotic I or II nuclear divisions, forming syncytial secondary spermatocytes and spermatids. Abnormal cytokinetic cells develop sparse and dispersed midzone spindles during the early stage. However, during late stages, single and compact midzone spindles are formed as in normal cells, but localize asymmetrically and attach to the cortex. Myosin and f-actin were observed in the midzone spindle and midbody regions of normally cleaving cells as well as in those cells that failed to develop a cytokinetic furrow, implying that cytokinetic failure is unlikely to be due to defect in myosin or actin assembly. Depolymerization of microtubules by nocodazole resulted in the loss of the midbody-associated f-actin and myosin. These observations suggest that actin-myosin localization in the midbody could be a microtubule-dependent process that may not play a direct role in cytokinetic furrowing. Anti-centrin antibody labels the putative centrioles while anti-(gamma)-tubulin antibody labels the minus-ends of the midzone spindles of late-stage normal and abnormal cytokinetic cells, suggesting that the centrosome and midzone spindle nucleation in abnormal cytokinetic cells is not different from those of normally cleaving cells. Possible use of mouse male meiotic cells as a model system to study cytokinesis has been discussed.
利用针对细胞分裂装置各种成分的免疫荧光探针和电子显微镜技术研究了小鼠雄性减数分裂细胞分裂。在正常小鼠中，一些精母细胞在减数第一次或第二次核分裂后未能进行细胞分裂，形成多核的次级精母细胞和精子细胞。异常细胞分裂的细胞在早期会形成稀疏且分散的中带纺锤体。然而，在后期，会形成单个且紧密的中带纺锤体，如同正常细胞一样，但它们不对称定位并附着于皮质。在正常分裂细胞以及那些未能形成细胞分裂沟的细胞的中带纺锤体和中间体区域观察到了肌球蛋白和丝状肌动蛋白，这意味着细胞分裂失败不太可能是由于肌球蛋白或肌动蛋白组装缺陷所致。用诺考达唑使微管解聚导致与中间体相关的丝状肌动蛋白和肌球蛋白丢失。这些观察结果表明，肌动蛋白 - 肌球蛋白在中间体中的定位可能是一个依赖微管的过程，可能在细胞分裂沟形成中不发挥直接作用。抗中心粒蛋白抗体标记假定的中心粒，而抗γ - 微管蛋白抗体标记后期正常和异常细胞分裂细胞中带纺锤体的负端，这表明异常细胞分裂细胞中的中心体和中带纺锤体成核与正常分裂细胞并无差异。本文还讨论了将小鼠雄性减数分裂细胞用作研究细胞分裂的模型系统的可能性。
