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首页> 外文期刊>Biomolecules >Knockout of RNA Binding Protein MSI2 Impairs Follicle Development in the Mouse Ovary: Characterization of MSI1 and MSI2 during Folliculogenesis
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Knockout of RNA Binding Protein MSI2 Impairs Follicle Development in the Mouse Ovary: Characterization of MSI1 and MSI2 during Folliculogenesis

机译：RNA结合蛋白MSI2的基因敲除损害小鼠卵巢中的卵泡发育：卵泡形成过程中MSI1和MSI2的表征。

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Characterizing the mechanisms underlying follicle development in the ovary is crucial to understanding female fertility and is an area of increasing research interest. The RNA binding protein Musashi is essential for post-transcriptional regulation of oocyte maturation in Xenopus and is expressed during ovarian development in Drosophila. In mammals Musashi is important for spermatogenesis and male fertility, but its role in the ovary has yet to be characterized. In this study we determined the expression of mammalian Musashi proteins MSI1 and MSI2 during mouse folliculogenesis, and through the use of a MSI2-specific knockout mouse model we identified that MSI2 is essential for normal follicle development. Time-course characterization of MSI1 and MSI2 revealed distinct differences in steady-state mRNA levels and protein expression/localization at important developmental time-points during folliculogenesis. Using a gene-trap mouse model that inactivates Msi2, we observed a significant decrease in ovarian mass, and change in follicle-stage composition due to developmental blocking of antral stage follicles and pre-antral follicle loss through atresia. We also confirmed that hormonally stimulated Msi2-deficient mice produce significantly fewer MII oocytes (60.9% less than controls, p 0.05). Furthermore, the majority of these oocytes are of poor viability (62.2% non-viable/apoptotic, p 0.05), which causes a reduction in female fertility evidenced by decreased litter size in Msi2-deficient animals (33.1% reduction to controls, p 0.05). Our findings indicate that MSI1 and MSI2 display distinct expression profiles during mammalian folliculogenesis and that MSI2 is required for pre-antral follicle development.
机译：表征卵巢卵泡发育的潜在机制对于了解女性的生育能力至关重要，也是人们研究兴趣日增的领域。 RNA结合蛋白Musashi对于非洲爪蟾卵母细胞成熟的转录后调控至关重要，并在果蝇的卵巢发育过程中表达。在哺乳动物中，武藏对精子发生和雄性育性很重要，但其在卵巢中的作用尚待鉴定。在这项研究中，我们确定了小鼠卵泡形成过程中哺乳动物Musashi蛋白MSI1和MSI2的表达，并且通过使用MSI2特异性敲除小鼠模型，我们确定了MSI2对于正常卵泡发育至关重要。 MSI1和MSI2的时程表征揭示了卵泡形成过程中重要发育时间点的稳态mRNA水平和蛋白质表达/定位存在明显差异。使用灭活Msi2的基因陷阱小鼠模型，我们观察到卵巢质量显着减少，并且由于肛门前期卵泡的发育受阻以及通过闭锁而导致前期卵泡的损失，卵泡期组成发生了变化。我们还证实，激素刺激的Msi2缺陷型小鼠产生的MII卵母细胞明显更少（比对照组少60.9％，p <0.05）。此外，这些卵母细胞中的大多数生存能力较弱（62.2％无生命/凋亡，p <0.05），这导致雌性繁殖力下降，这是由Msi2缺陷型动物的产仔数减少所证实的（与对照组相比，减少33.1％，p <0.05）。我们的发现表明，MSI1和MSI2在哺乳动物卵泡形成过程中显示出不同的表达谱，而MSI2是前肛门卵泡发育所必需的。

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