MEI-1/katanin is required for translocation of the meiosis I spindle to the oocyte cortex in C elegans.
MEI-1/katanin is required for translocation of the meiosis I spindle to the oocyte cortex in C elegans.
复制标题
MEI-1/katanin 是线虫减数分裂 I 纺锤体易位至卵母细胞皮质所必需的。
DOI：
10.1016/s0012-1606(03)00216-1
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发表时间：
2003
影响因子：
2.7
通讯作者：
McNally,FrancisJ
中科院分区：
文献类型：
--
作者：
Yang,Hsin-ya;McNally,Karen;McNally,FrancisJ
在大多数动物中，雌性减数分裂染色体的成功分离包括减数分裂I和减数分裂II纺锤体与细胞皮质的顺序结合，以便额外的染色体可以沉积在极体中。由此导致的染色体数量的减少对于防止受精后产生多倍体胚胎至关重要。利用含有荧光标记的染色体或微管的线虫活卵母细胞的时间推移成像，我们表征了减数分裂纺锤体相对于细胞皮质的运动。纺锤体组件从皮层启动了几个微米。在形成两极结构后，减数分裂I纺锤体移位到皮层。当微管部分耗尽时，二价染色体向皮质的移位被阻止，而不影响细胞周期的计时。在缺乏微管切断酶MeI-1的卵母细胞中，纺锤体移动到皮质，但与皮质的联系不稳定。与野生型纺锤体的易位不同，Mei-1缺失的纺锤体的运动依赖于FZY-1/CDC20，FZY-1/CDC20是中期/后期转换的调节因子。我们在野生型胚胎和mei-1突变胚胎减数分裂过程中观察到微管和依赖FZY-1/CDC20的环状胞质流动。我们认为，在mei-1突变卵母细胞中，这种细胞质流动足以驱动纺锤体进入皮质。细胞质流动不是正常的纺锤体易位机制，因为在没有细胞质流动的胚胎中发生了易位，去除了Orbit/CLASP同源基因、CLS-2或FZY-1的胚胎。这些结果表明，微管切断在减数分裂纺锤体移位到皮层中起着直接作用。
In most animals, successful segregation of female meiotic chromosomes involves sequential associations of the meiosis I and meiosis II spindles with the cell cortex so that extra chromosomes can be deposited in polar bodies. The resulting reduction in chromosome number is essential to prevent the generation of polyploid embryos after fertilization. Using time-lapse imaging of living Caenorhabditis elegans oocytes containing fluorescently labeled chromosomes or microtubules, we have characterized the movements of meiotic spindles relative to the cell cortex. Spindle assembly initiated several microns from the cortex. After formation of a bipolar structure, the meiosis I spindle translocated to the cortex. When microtubules were partially depleted, translocation of the bivalent chromosomes to the cortex was blocked without affecting cell cycle timing. In oocytes depleted of the microtubule-severing enzyme, MEI-1, spindles moved to the cortex, but association with the cortex was unstable. Unlike translocation of wild-type spindles, movement of MEI-1-depleted spindles was dependent on FZY-1/CDC20, a regulator of the metaphase/anaphase transition. We observed a microtubule and FZY-1/CDC20-dependent circular cytoplasmic streaming in wild-type and mei-1 mutant embryos during meiosis. We propose that, in mei-1 mutant oocytes, this cytoplasmic streaming is sufficient to drive the spindle into the cortex. Cytoplasmic streaming is not the normal spindle translocation mechanism because translocation occurred in the absence of cytoplasmic streaming in embryos depleted of either the orbit/CLASP homolog, CLS-2, or FZY-1. These results indicate a direct role of microtubule severing in translocation of the meiotic spindle to the cortex.