BCAS2 is involved in alternative splicing and mouse oocyte development.
BCAS2 is involved in alternative splicing and mouse oocyte development.
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BCAS2 参与选择性剪接和小鼠卵母细胞发育。
DOI：
10.1096/fj.202101279r
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发表时间：
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影响因子：
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通讯作者：
Li Lei
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作者：
Zhang Jiaqi;Liu Wenbo;Li Guangyue;Xu Chengpeng;Nie Xiaoqing;Qin D;an;Wang Qizhi;Lu Xukun;Liu Jianqiao;Li Lei
选择性剪接（alternative splicing，AS）是调控器官发生和生育的重要机制。乳腺癌扩增序列2（BCAS2）是PRP19复合物的核心组成部分之一，是一种具有剪接功能的复合物，通过调节AS参与雄性小鼠减数分裂的启动。然而，BCAS2在小鼠卵子发生中的作用在很大程度上仍然未知。在本研究中，我们发现Bcas2在原始卵泡的卵母细胞中高表达，Vasa‐Cre‐介导的Bcas2缺失导致卵母细胞质量下降，卵子发生和卵泡发育异常。小鼠卵母细胞Bcas2的缺失导致了991个AS事件的改变，这些AS事件对应于706个基因，包括Pabpc 11、Nobox、Zfp207、Mybl 2、Prc 1和Spc 25，这些基因与卵子发生和纺锤体组装有关。此外，BCAS2的破坏导致小鼠卵母细胞中PRP 19核心蛋白的降解。提示BCAS2可能通过PRP19复合物参与小鼠卵母细胞发育过程中功能基因的AS。
Alternative splicing (AS) is an important mechanism to regulate organogenesis and fertility. Breast carcinoma amplified sequence 2 (BCAS2) is one of the core components of the PRP19 complex, a multiple function complex including splicing, and it is involved in the initiation of meiosis through regulating AS in male mice. However, the role of BCAS2 in mouse oogenesis remains largely unknown. In this study, we found that BCAS2 was highly expressed in the oocytes of primordial follicles.Vasa‐Cre‐mediated deletion ofBcas2caused poor oocyte quality, abnormal oogenesis and follicular development. The deletion ofBcas2in mouse oocytes caused alteration in 991 AS events that corresponded to 706 genes, includingPabpc1l,Nobox,Zfp207,Mybl2,Prc1, andSpc25, which were associated with oogenesis and spindle assembly. Moreover, the disruption of BCAS2 led to degradation of PRP19 core proteins in mouse oocytes. These results suggested that BCAS2 was involved in the AS of functional genes through PRP19 complex during mouse oocyte development.