Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis

Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis
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DOI:
10.1101/gad.536109
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发表时间:
2009-09-15
影响因子:
10.5
通讯作者:
Hoffmann, Eva
Hoffmann, Eva
中科院分区:
生物学1区
文献类型:
--
作者:
Jordan, Philip;Copsey, Alice;Hoffmann, Eva

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在有丝分裂和减数分裂细胞中,几种蛋白激酶协同协调和整合G2/M转变中的细胞和染色体事件。在减数分裂的G2/M过渡过程中,包括完成交叉重组、纺锤体的形成和联会复合体(SC)的破裂。我们发现Ipl1/Aurora B是SC分解的主要调节因子。缺乏Ipl1或其激酶活性的突变体可以正常的时间组装SCs,但不能及时将中心元件组分ZIP1及其结合伙伴Smt3/SUMO从染色体上分离出来。此外,Ipl1活性的缺乏导致了CDC5和CDC5诱导的ndt80突变体中SC拆解的延迟。Ipl1突变体中的交叉水平与野生型中观察到的相似,表明完全的SC分解不是联合分子解析和随后的交叉形成的先决条件。此外,减数分裂I和减数分裂II特异的B型细胞周期蛋白的表达在Ipl1突变体中正常存在,尽管后期I纺锤体的形成延迟。这些观察结果表明,在减数分裂前期结束时,Ipl1通过分辨交叉和细胞周期进程来协调减数分裂染色体结构的变化。
Several protein kinases collaborate to orchestrate and integrate cellular and chromosomal events at the G2/M transition in both mitotic and meiotic cells. During the G2/M transition in meiosis, this includes the completion of crossover recombination, spindle formation, and synaptonemal complex (SC) breakdown. We identified Ipl1/Aurora B kinase as the main regulator of SC disassembly. Mutants lacking Ipl1 or its kinase activity assemble SCs with normal timing, but fail to dissociate the central element component Zip1, as well as its binding partner, Smt3/SUMO, from chromosomes in a timely fashion. Moreover, lack of Ipl1 activity causes delayed SC disassembly in a cdc5 as well as a CDC5-inducible ndt80 mutant. Crossover levels in the ipl1 mutant are similar to those observed in wild type, indicating that full SC disassembly is not a prerequisite for joint molecule resolution and subsequent crossover formation. Moreover, expression of meiosis I and meiosis II-specific B-type cyclins occur normally in ipl1 mutants, despite delayed formation of anaphase I spindles. These observations suggest that Ipl1 coordinates changes to meiotic chromosome structure with resolution of crossovers and cell cycle progression at the end of meiotic prophase.