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Mutations in the Chromosomal Passenger Complex and the Condensin Complex Differentially Affect Synaptonemal Complex Disassembly and Metaphase I Configuration in Drosophila Female Meiosis

机译:在果蝇女性减数分裂中染色体乘客复合物和凝缩蛋白复合物的突变差异影响突触复合物的分解和中期I构型。

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摘要

Production of haploid gametes relies on the specially regulated meiotic cell cycle. Analyses of the role of essential mitotic regulators in meiosis have been hampered by a shortage of appropriate alleles in metazoans. We characterized female-sterile alleles of the condensin complex component dcap-g and used them to define roles for condensin in Drosophila female meiosis. In mitosis, the condensin complex is required for sister-chromatid resolution and contributes to chromosome condensation. In meiosis, we demonstrate a role for dcap-g in disassembly of the synaptonemal complex and for proper retention of the chromosomes in a metaphase I-arrested state. The chromosomal passenger complex also is known to have mitotic roles in chromosome condensation and is required in some systems for localization of the condensin complex. We used the QA26 allele of passenger component incenp to investigate the role of the passenger complex in oocyte meiosis. Strikingly, in incenpQA26 mutants maintenance of the synaptonemal complex is disrupted. In contrast to the dcap-g mutants, the incenp mutation leads to a failure of paired homologous chromosomes to biorient, such that bivalents frequently orient toward only one pole in prometaphase and metaphase I. We show that incenp interacts genetically with ord, suggesting an important functional relationship between them in meiotic chromosome dynamics. The dcap-g and incenp mutations cause maternal effect lethality, with embryos from mutant mothers arrested in the initial mitotic divisions.
机译:单倍体配子的产生依赖于特别调节的减数分裂细胞周期。由于后生动物中缺乏适当的等位基因,阻碍了有丝分裂调节剂在减数分裂中的作用分析。我们表征了凝缩蛋白复杂成分dcap-g的雌性不育等位基因,并用它们来定义凝缩蛋白在果蝇雌性减数分裂中的作用。在有丝分裂中,凝缩蛋白复合物是姐妹染色单体解析所必需的,并且有助于染色体凝缩。在减数分裂中,我们证明了dcap-g在突触复合物的拆卸中和染色体在中期I停滞状态下的适当保留中的作用。还已知染色体客体复合物在染色体凝结中具有有丝分裂作用,并且在某些系统中对于凝缩蛋白复合物的定位是必需的。我们使用乘客成分的QA26等位基因来研究乘客复合体在卵母细胞减数分裂中的作用。令人惊讶的是,在incenpQA26突变体中,突触复合物的维持被破坏了。与dcap-g突变体相反,incenp突变导致成对的同源染色体无法进行生物定向,因此二价体常在前中期和中期I方向仅定向于一个极。我们证明了incenp与ord发生了遗传相互作用,这表明一个重要的发现它们之间在减数分裂染色体动力学中的功能关系。 dcap-g和incep突变引起母体杀伤力,来自突变母亲的胚胎在最初的有丝分裂分裂中被捕。

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