The ran GTPase mediates chromatin signaling to control cortical polarity during polar body extrusion in mouse oocytes
The ran GTPase mediates chromatin signaling to control cortical polarity during polar body extrusion in mouse oocytes
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DOI：
10.1016/j.devcel.2006.11.008
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发表时间：
2007-02-01
影响因子：
11.8
通讯作者：
Li, Rong
中科院分区：
文献类型：
--
作者：
Deng, Manqi;Suraneni, Praveen;Li, Rong
哺乳动物卵母细胞不对称减数分裂产生成熟卵子和极体的分子基础仍然知之甚少。先前的研究表明，小鼠卵母细胞减数分裂染色体的不对称定位提供了皮质极性的线索。在这里，我们表明，染色质诱导的皮质反应可以完全重建注射DNA包被珠中期II逮捕的鸡蛋。注射的DNA珠诱导皮质肌动蛋白帽，周围的肌球蛋白II环，在某种程度上，取决于珠的数量和它们与皮质的距离。Ran GTdR在这一过程中起着关键作用，因为显性负性和组成性活性Ran突变体破坏DNA诱导的皮层极化。RAN介导的信号传导到皮质是独立的纺锤体，但需要皮质肌球蛋白II组装。我们假设Ran（GTP）梯度作为分子标尺来解释减数分裂染色质的不对称位置。
The molecular basis for asymmetric meiotic divisions in mammalian oocytes that give rise to mature eggs and polar bodies remains poorly understood. Previous studies demonstrated that the asymmetrically positioned meiotic chromosomes provide the cue for cortical polarity in mouse oocytes. Here we show that the chromatin-induced cortical response can be fully reconstituted by injecting DNA-coated beads into metaphase II-arrested eggs. The injected DNA beads induce a cortical actin cap, surrounded by a myosin II ring, in a manner that depends on the number of beads and their distance from the cortex. The Ran GTPase plays a critical role in this process, because dominant-negative and constitutively active Ran mutants disrupt DNA-induced cortical polarization. The Ran-mediated signaling to the cortex is independent of the spindle but requires cortical myosin II assembly. We hypothesize that a Ran(GTP) gradient serves as a molecular ruler to interpret the asymmetric position of the meiotic chromatin.