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A Genetic Screen for Dominant Enhancers of the Cell-Cycle Regulator α-Endosulfine Identifies Matrimony as a Strong Functional Interactor in Drosophila

机译:遗传筛选的细胞周期调节器α-硫代的主要增强子确定婚姻为果蝇中的强大功能相互作用者。

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摘要

The coordination of cell-cycle events with developmental processes is essential for the reproductive success of organisms. In Drosophila melanogaster, meiosis is tightly coupled to oocyte development, and early embryos undergo specialized S-M mitoses that are supported by maternal products. We previously showed that the small phosphoprotein α-endosulfine (Endos) is required for normal oocyte meiotic maturation and early embryonic mitoses in Drosophila. In this study, we performed a genetic screen for dominant enhancers of and identified several genomic regions that, when deleted, lead to impaired fertility of endos00003/+ heterozygous females. We uncovered (), which encodes a Polo kinase inhibitor, as a strong dominant enhancer of . mtrm126 +/+ endos00003 females are sterile because of defects in early embryonic mitoses, and this phenotype is reverted by removal of one copy of . These results provide compelling genetic evidence that excessive Polo activity underlies the strong functional interaction between and . Moreover, we show that is required for the increased expression of Mtrm in mature oocytes, which is presumably loaded into early embryos. These data are consistent with the model that maternal antagonizes Polo function in the early embryo to ensure normal mitoses through its effects on Mtrm expression during late oogenesis. Finally, we also identified genomic deletions that lead to loss of viability of endos00003/+ heterozygotes, consistent with recently published studies showing that is required zygotically to regulate the cell cycle during development.
机译:细胞周期事件与发育过程的协调对于有机体的生殖成功至关重要。在果蝇中,减数分裂与卵母细胞的发育紧密相关,并且早期的胚胎经历由母体产物支持的专门的S-M有丝分裂。我们以前表明,果蝇正常卵母细胞减数分裂成熟和早期胚胎有丝分裂所需要的小磷蛋白α-硫丹(Endos)。在这项研究中,我们对的显性增强子进行了遗传筛选,并鉴定了几个基因组区域,这些区域被删除后会导致内吞 00003 / +杂合子雌性的生育力受损。我们发现()编码Polo激酶抑制剂,是的强大的显性增强剂。 mtrm 126 + / + endos 00003 雌性由于早期胚胎有丝分裂中的缺陷而变得不育,并且通过去除1个拷贝即可恢复该表型。这些结果提供了令人信服的遗传学证据,表明过度的Polo活动构成了和之间强烈的功能相互作用。此外,我们表明,Mtrm在成熟卵母细胞中表达的增加是必需的,它可能被装载到早期胚胎中。这些数据与母体拮抗早期胚胎中的Polo功能以通过其在后期卵子形成过程中对Mtrm表达的影响确保正常有丝分裂的模型一致。最后,我们还鉴定了导致内吞 00003 / +杂合子丧失活力的基因组缺失,这与最近发表的研究表明在发育过程中需要合子调节细胞周期的研究一致。

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