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A Tudor Domain Protein SPINDLIN1 Interacts with the mRNA-Binding Protein SERBP1 and Is Involved in Mouse Oocyte Meiotic Resumption

机译:Tudor域蛋白SPINDLIN1与mRNA结合蛋白SERBP1相互作用并参与小鼠卵母细胞减数分裂的恢复。

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摘要

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.
机译:哺乳动物卵母细胞停在减数分裂的前期I,并在排卵前恢复减数分裂。减数分裂阻滞和恢复的协调部分取决于母本转录本的转录后调控。在这里,我们报告,SPINDLIN1(SPIN1),一种含有Tudor样结构域的母体蛋白,与已知的mRNA结合蛋白SERBP1相互作用,并参与调节母体转录本以控制减数分裂的恢复。缺乏Spin1的小鼠卵母细胞经历正常的卵泡形成,但在恢复减数分裂中存在缺陷。 SPIN1通过其Tudor样结构域与SERBP1形成核糖核蛋白复合物,并调节mRNA的稳定性和/或翻译。在Spin1突变卵母细胞中,cAMP降解酶PDE3A的mRNA减少,这可能导致减数分裂停滞。我们的研究表明Spin1在转录后调控母本转录,并参与减数分裂的恢复。

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