摘要
哺乳动物卵母细胞进行减数分裂时进行两次连续的不对称性分裂,最终形成一个体积较大的卵子和两个体积较小的极体。这种不对称性分裂对卵母细胞以及胚胎发育有很重要的作用。各种与纺锤体移位及锚定和收缩环的形成、极体排出有关的因子,例如肌动蛋白相关蛋白2/3(Arp2/3)复合物、JMY、小三磷酸鸟苷(GTP)酶即激活肌动蛋白成核因子等之间相互作用形成一个调节卵母细胞不对称性分裂的信号通路。然而老化的卵母细胞中皮质极化消失,成核促进因子及相关调控因子的水平和活性下降,最终导致老化卵母细胞的受精率及受精后的卵裂率等明显下降。综述老化卵母细胞减数分裂时不对称性丧失的研究进展。
Mammalian oocyte meiosis encompasses two consecutive rounds of asymmetric divisions to generate one big egg and ,as by-products ,two small polar bodies. This asymmetric division is crucial for the oocyte and embryonic development. The interaction between various factors associated with spindle positioning, the formation of myosin ring and extrusion of the first polar body,such as actin-related protein 2/3 (Arp2/3) complex,JMY,small GTPase (actin nucleation activation factor),forms the signal pathways regulating the asymmetrical division of oocyte. However,it is found that the aged oocyte shows loss of oocyte cortical polarity, reduction of the nucleation-promoting factors and related regulatory factors and their activities, resulting in the decreased rate of fertilization and then rate of cleavage in aged oocyte. We reviewed the progression of research on loss of asymmetry during meiotic division in aged oocytes.
出处
《国际生殖健康/计划生育杂志》
CAS
2014年第5期384-387,共4页
Journal of International Reproductive Health/Family Planning