Department of Animal Sciences, Chungbuk National University, Cheongju 361-763, Korea.
Mol Hum Reprod. 2011 May;17(5):296-304. doi: 10.1093/molehr/gar006. Epub 2011 Jan 25.
JMY is a transcriptional co-factor of p53. Latest work has revealed that JMY is also an actin nucleation factor that regulates new filament assembly and activates Arp2/3 complex in somatic cells; however, roles of JMY in mouse oocyte are unknown. Here we showed the expression and functions of JMY during mouse oocyte meiotic maturation. JMY mRNA is expressed largely from germinal vesicle to metaphase I stage, and gradually decreased during anaphase I, telophase I (TI) and metaphase II (MII) stages. Immunostaining results showed that JMY localized at the spindle and cytoplasm of oocytes. Depletion of JMY by RNAi resulted in symmetric division, failure of spindle migration and cytokinesis during oocyte meiotic maturation, showing a 2-cell-like MII oocyte and TI stage arrest. Actin cap and cortical granules-free domain formation were also disrupted after JMY RNAi, indicating the failure of spindle migration. JMY antibody injection results were consistent with those of JMY RNAi, further confirming the involvement of JMY in oocyte polarity. Our data indicate that JMY is required for spindle migration, asymmetric division and cytokinesis during mouse oocyte maturation.
JMY 是 p53 的转录共因子。最新研究表明，JMY 也是一种肌动蛋白成核因子，可调节体细胞中新丝的组装并激活 Arp2/3 复合物；然而，JMY 在小鼠卵母细胞中的作用尚不清楚。在这里，我们研究了 JMY 在小鼠卵母细胞减数分裂成熟过程中的表达和功能。JMY mRNA 主要从生发泡期表达到中期 I 期，在后期 I 期、末期 I（TI）和中期 II（MII）期逐渐减少。免疫染色结果表明 JMY 定位于卵母细胞的纺锤体和细胞质中。用 RNAi 耗尽 JMY 会导致卵母细胞减数分裂成熟过程中的对称分裂、纺锤体迁移和胞质分裂失败，表现为 2 细胞样的 MII 卵母细胞和 TI 期阻滞。JMY RNAi 后还会破坏肌动蛋白帽和皮质颗粒无区的形成，表明纺锤体迁移失败。JMY 抗体注射的结果与 JMY RNAi 的结果一致，进一步证实了 JMY 参与卵母细胞极性的形成。我们的数据表明，JMY 是小鼠卵母细胞成熟过程中纺锤体迁移、不对称分裂和胞质分裂所必需的。
