Mammalian Development Laboratory, Institute of Medical Biology, A-STAR, Singapore, Singapore.
PLoS One. 2013 Jul 22;8(7):e69764. doi: 10.1371/journal.pone.0069764. Print 2013.
Mammalian oocytes are arrested at prophase I of meiosis, and resume meiosis prior to ovulation. Coordination of meiotic arrest and resumption is partly dependent on the post-transcriptional regulation of maternal transcripts. Here, we report that, SPINDLIN1 (SPIN1), a maternal protein containing Tudor-like domains, interacts with a known mRNA-binding protein SERBP1, and is involved in regulating maternal transcripts to control meiotic resumption. Mouse oocytes deficient for Spin1 undergo normal folliculogenesis, but are defective in resuming meiosis. SPIN1, via its Tudor-like domain, forms a ribonucleoprotein complex with SERBP1, and regulating mRNA stability and/or translation. The mRNA for the cAMP-degrading enzyme, PDE3A, is reduced in Spin1 mutant oocytes, possibly contributing to meiotic arrest. Our study demonstrates that Spin1 regulates maternal transcripts post-transcriptionally and is involved in meiotic resumption.
哺乳动物卵母细胞在减数分裂前期 I 期停滞，并在排卵前恢复减数分裂。减数分裂停滞和恢复的协调部分依赖于母体转录物的转录后调控。在这里，我们报告说，含有 Tudor 样结构域的母体蛋白 SPINDLIN1（SPIN1）与已知的 mRNA 结合蛋白 SERBP1 相互作用，并参与调节母体转录物以控制减数分裂恢复。Spin1 缺失的小鼠卵母细胞经历正常的卵泡发生，但在恢复减数分裂方面存在缺陷。SPIN1 通过其 Tudor 样结构域与 SERBP1 形成核糖核蛋白复合物，调节 mRNA 稳定性和/或翻译。cAMP 降解酶 PDE3A 的 mRNA 在 Spin1 突变体卵母细胞中减少，可能导致减数分裂停滞。我们的研究表明，Spin1 在后转录水平调节母体转录物，并参与减数分裂恢复。
