Sister chromatid cohesion, mediated by cohesin complex and established by the acetyltransferases Esco1 and Esco2, is essential for faithful chromosome segregation. Mutations in Esco2 cause Roberts syndrome, a developmental disease characterized by severe prenatal retardation as well as limb and facial abnormalities. However, its exact roles during oocyte meiosis have not clearly defined. Here, we report that Esco2 localizes to the chromosomes during oocyte meiotic maturation. Depletion of Esco2 by morpholino microinjection leads to the precocious polar body extrusion, the escape of metaphase I arrest induced by nocodazole treatment and the loss of BubR1 from kinetochores, indicative of inactivated SAC. Furthermore, depletion of Esco2 causes a severely impaired spindle assembly and chromosome alignment, accompanied by the remarkably elevated incidence of defective kinetochore-microtubule attachments which consequently lead to the generation of aneuploid eggs. Notably, we find that the involvement of Esco2 in SAC and kinetochore functions is mediated by its binding to histone H4 and acetylation of H4K16 both in vivo and in vitro. Thus, our data assign a novel meiotic function to Esco2 beyond its role in the cohesion establishment during mouse oocyte meiosis.

中文翻译：

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黏附素乙酰转移酶Esco2通过在小鼠卵母细胞减数分裂过程中维持H4K16乙酰化作用来调节SAC和线粒体功能

姊妹染色单体凝聚力，是由凝聚素复合物介导并由乙酰转移酶Esco1和Esco2建立的，对于忠实的染色体分离至关重要。Esco2的突变会导致罗伯茨综合症，这是一种以严重的产前发育迟缓以及四肢和面部异常为特征的发育性疾病。但是，其在卵母细胞减数分裂中的确切作用尚未明确。在这里，我们报告Esco2定位于卵母细胞减数分裂成熟过程中的染色体。通过吗啉代显微注射耗尽Esco2会导致性早熟的极体挤出，诺考达唑处理诱导的I期中期捕获的逃逸以及动植物中BubR1的丢失，这表明SAC处于灭活状态。此外，Esco2的耗竭会严重损害纺锤体组装和染色体排列，伴随着动球体微管附件缺陷的发生率显着升高，从而导致产生非整倍体卵。值得注意的是，我们发现Esco2参与SAC和线粒体功能是通过其与组蛋白H4的结合和H4K16的乙酰化而介导的体内和体外。因此，我们的数据为Esco2赋予了一种新的减数分裂功能，超越了它在小鼠卵母细胞减数分裂过程中建立内聚力的作用。