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首页> 外文期刊>Journal of Cell Science >Overexpression of SETβ, a protein localizing to centromeres, causes precocious separation of chromatids during the first meiosis of mouse oocytes
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Overexpression of SETβ, a protein localizing to centromeres, causes precocious separation of chromatids during the first meiosis of mouse oocytes

机译：SETβ（一种定位于着丝粒的蛋白）的过表达会在小鼠卵母细胞的第一次减数分裂期间导致染色单体的过早分离

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Chromosome segregation in mammalian oocyte meiosis is an error-prone process, and any mistake in this process may result in aneuploidy, which is the main cause of infertility, abortion and many genetic diseases. It is now well known that shugoshin and protein phosphatase 2A (PP2A) play important roles in the protection of centromeric cohesion during the first meiosis. PP2A can antagonize the phosphorylation of rec8, a member of the cohesin complex, at the centromeres and thus prevent cleavage of rec8 and so maintain the cohesion of chromatids. SETβ is a protein that physically interacts with shugoshin and inhibits PP2A activity. We thus hypothesized that SETβ might regulate cohesion protection and chromosome segregation during oocyte meiotic maturation. Here we report for the first time the expression, subcellular localization and functions of SETβ during mouse oocyte meiosis. Immunoblotting analysis showed that the expression level of SETβ was stable from the germinal vesicle stage to the MII stage of oocyte meiosis. Immunofluorescence analysis showed SETβ accumulation in the nucleus at the germinal vesicle stage, whereas it was targeted mainly to the inner centromere area and faintly localized to the interchromatid axes from germinal vesicle breakdown to MI stages. At the MII stage, SETβ still localized to the inner centromere area, but could relocalize to kinetochores in a process perhaps dependent on the tension on the centromeres. SETβ partly colocalized with PP2A at the inner centromere area. Overexpression of SETβ in mouse oocytes caused precocious separation of sister chromatids, but depletion of SETβ by RNAi showed little effects on the meiotic maturation process. Taken together, our results suggest that SETβ, even though it localizes to centromeres, might not be essential for chromosome separation during mouse oocyte meiotic maturation, although its forced overexpression causes premature chromatid separation.
机译：哺乳动物卵母细胞减数分裂中的染色体分离是一个容易出错的过程，该过程中的任何错误都可能导致非整倍性，这是不育，流产和许多遗传疾病的主要原因。众所周知，在第一个减数分裂过程中，守护甜心素和蛋白磷酸酶2A（PP2A）在保护着丝粒凝聚方面起着重要作用。 PP2A可以拮抗着丝粒复合体成员rec8的磷酸化，从而阻止rec8的裂解，从而保持染色单体的内聚。 SETβ是一种蛋白质，与Shugoshin发生物理相互作用，并抑制PP2A活性。因此，我们假设SETβ可能在卵母细胞减数分裂成熟过程中调节内聚保护和染色体分离。在这里，我们首次报道小鼠卵母细胞减数分裂过程中SETβ的表达，亚细胞定位和功能。免疫印迹分析表明，SETβ的表达水平在卵母细胞减数分裂的生小泡阶段到MII阶段是稳定的。免疫荧光分析显示，SETβ在生小泡阶段聚集在细胞核中，而它主要靶向于着丝粒内部区域，并微弱地定位于从生小泡破裂到MI阶段的染色体间轴。在MII阶段，SETβ仍位于着丝粒内部区域，但可能在一定程度上取决于着丝粒的张力而重新定位到动植物。 SETβ在内部着丝粒区域与PP2A部分共定位。小鼠卵母细胞中SETβ的过表达引起姐妹染色单体的过早分离，但RNAi清除SETβ对减数分裂成熟过程几乎没有影响。综上所述，我们的研究结果表明，尽管SETβ定位于着丝粒，但它在小鼠卵母细胞减数分裂成熟过程中的染色体分离可能不是必不可少的，尽管它的强制过度表达会导致过早的染色单体分离。

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