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Two pathways regulate cortical granule translocation to prevent polyspermy in mouse oocytes.

机译:两种途径调节皮质颗粒易位以防止小鼠卵母细胞中的多精症。

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摘要

An egg must be fertilized by a single sperm only. To prevent polyspermy, the zona pellucida, a structure that surrounds mammalian eggs, becomes impermeable upon fertilization, preventing the entry of further sperm. The structural changes in the zona upon fertilization are driven by the exocytosis of cortical granules. These translocate from the oocyte’s centre to the plasma membrane during meiosis. However, very little is known about the mechanism of cortical granule translocation. Here we investigate cortical granule transport and dynamics in live mammalian oocytes by using Rab27a as a marker. We show that two separate mechanisms drive their transport: myosin Va-dependent movement along actin filaments, and an unexpected vesicle hitchhiking mechanism by which cortical granules bind to Rab11a vesicles powered by myosin Vb. Inhibiting cortical granule translocation severely impaired the block to sperm entry, suggesting that translocation defects could contribute to miscarriages that are caused by polyspermy.
机译:卵只能由一个精子受精。为了防止多精子,透明带(围绕哺乳动物卵的结构)在受精后变得不可渗透,从而阻止了其他精子的进入。受精后透明带的结构变化是由皮质颗粒的胞吐作用驱动的。这些细胞在减数分裂过程中从卵母细胞的中心转移到质膜。但是,对皮质颗粒移位的机制了解甚少。在这里,我们通过使用Rab27a作为标记物来研究哺乳动物活卵母细胞中皮质颗粒的运输和动力学。我们显示了两个独立的机制驱动其运输:沿肌动蛋白丝的肌球蛋白Va依赖运动,和意外的囊泡搭便车机制,通过这种机制皮层颗粒结合由肌球蛋白Vb驱动的Rab11a囊泡。抑制皮质颗粒易位严重损害了精子进入的阻滞,表明易位缺陷可能导致由多精子引起的流产。

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