akirin is required for diakinesis bivalent structure and synaptonemal complex disassembly at meiotic prophase I.
akirin is required for diakinesis bivalent structure and synaptonemal complex disassembly at meiotic prophase I.
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akirin是减数分裂前期 I 的二分裂二价结构和突触复合体解体所必需的。
DOI：
10.1091/mbc.e12-11-0841
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发表时间：
2013-04
影响因子：
3.3
通讯作者：
Smolikove S
中科院分区：
文献类型：
--
作者：
Clemons AM;Brockway HM;Yin Y;Kasinathan B;Butterfield YS;Jones SJ;Colaiácovo MP;Smolikove S
减数分裂的准确进行需要形成浓缩的和适当重塑的二价体。减数分裂的作用被确定为高度进化上保守的蛋白AKIRIN在二价重塑联会复合体（SC）依赖和SC独立的方式，表明适当的SC拆卸是至关重要的二价结构。在减数分裂过程中，进化上保守的机制调节染色体重塑，导致形成紧密的二价结构。这种二价体是一对相连的同源染色体，在减数分裂中对染色体的正确分离是必不可少的。紧密二价体的形成涉及染色体浓缩和围绕交换的重组。联会复合体（SC），它介导的同源染色体协会前交叉形成，拆卸同时增加凝聚在二价重塑。染色体浓缩和SC解体可能是获得功能性二价结构的关键步骤。然而，控制SC分解的机制仍不清楚。在这里，我们确定akir-1作为一个基因参与的关键事件减数分裂前期I在秀丽隐杆线虫。AKIR-1是一种在后生动物中保守的蛋白质，在减数分裂中缺乏任何先前已知的功能。我们发现，akir-1突变体表现出严重的减数分裂缺陷后期前期I，包括不正确的解体的SC和异常的染色体凝聚，独立的凝聚素复合物。这些后期-前期缺陷然后导致二价体的异常重构。akir-1突变体的减数分裂延迟，并伴有落后染色体。因此，我们的分析提供了证据的重要作用，适当的SC拆卸配置功能的二价结构。
Formation of a condensed and properly remodeled bivalent is required for accurate execution of meiosis. Meiotic roles are identified for the highly evolutionarily conserved protein AKIRIN in bivalent remodeling in a synaptonemal complex (SC)–dependent and SC–independent manner, demonstrating that proper SC disassembly is crucial for bivalent structure. During meiosis, evolutionarily conserved mechanisms regulate chromosome remodeling, leading to the formation of a tight bivalent structure. This bivalent, a linked pair of homologous chromosomes, is essential for proper chromosome segregation in meiosis. The formation of a tight bivalent involves chromosome condensation and restructuring around the crossover. The synaptonemal complex (SC), which mediates homologous chromosome association before crossover formation, disassembles concurrently with increased condensation during bivalent remodeling. Both chromosome condensation and SC disassembly are likely critical steps in acquiring functional bivalent structure. The mechanisms controlling SC disassembly, however, remain unclear. Here we identify akir-1 as a gene involved in key events of meiotic prophase I in Caenorhabditis elegans. AKIR-1 is a protein conserved among metazoans that lacks any previously known function in meiosis. We show that akir-1 mutants exhibit severe meiotic defects in late prophase I, including improper disassembly of the SC and aberrant chromosome condensation, independently of the condensin complexes. These late-prophase defects then lead to aberrant reconfiguring of the bivalent. The meiotic divisions are delayed in akir-1 mutants and are accompanied by lagging chromosomes. Our analysis therefore provides evidence for an important role of proper SC disassembly in configuring a functional bivalent structure.