首页> 外文期刊>Genes and Development: a Journal Devoted to the Molecular Analysis of Gene Expression in Eukaryotes, Prokaryotes, and Viruses >Crossovers trigger a remodeling of meiotic chromosome axis composition that is linked to two-step loss of sister chromatid cohesion.
【24h】

Crossovers trigger a remodeling of meiotic chromosome axis composition that is linked to two-step loss of sister chromatid cohesion.

机译:交叉触发减数分裂染色体轴组成的重塑,这与姐妹染色单体内聚力的两步损失有关。

获取原文
获取原文并翻译 | 示例
           

摘要

Segregation of homologous chromosomes during meiosis depends on linkages (chiasmata) created by crossovers and on selective release of a subset of sister chromatid cohesion at anaphase I. During Caenorhabditis elegans meiosis, each chromosome pair forms a single crossover, and the position of this event determines which chromosomal regions will undergo cohesion release at anaphase I. Here we provide insight into the basis of this coupling by uncovering a large-scale regional change in chromosome axis composition that is triggered by crossovers. We show that axial element components HTP-1 and HTP-2 are removed during late pachytene, in a crossover-dependent manner, from the regions that will later be targeted for anaphase I cohesion release. We demonstrate correspondence in position and number between chiasmata and HTP-1/2-depleted regions and provide evidence that HTP-1/2 depletion boundaries mark crossover sites. In htp-1 mutants, diakinesis bivalents lack normal asymmetrical features, and sister chromatid cohesion is prematurely lost during the meiotic divisions. We conclude that HTP-1 is central to the mechanism linking crossovers with late-prophase bivalent differentiation and defines the domains where cohesion will be protected until meiosis II. Further, we discuss parallels between the pattern of HTP-1/2 removal in response to crossovers and the phenomenon of crossover interference.
机译:减数分裂过程中同源染色体的分离取决于交叉产生的连锁(chiasmata)以及在后期I选择性释放姐妹染色单体凝聚的子集。在秀丽隐杆线虫减数分裂期间,每个染色体对形成单个交换,并且该事件的位置决定了哪些染色体区域将在后期I发生凝聚释放。在这里,我们通过揭示跨界触发的染色体轴组成的大规模区域变化,为这种耦合的基础提供了见识。我们显示轴向元素成分HTP-1和HTP-2在后期粗线期以交叉依赖的方式从后期将被靶向后期I内聚释放的区域中删除。我们证明了位置和数量与光斑和HTP-1 / 2耗尽区域之间的对应关系,并提供了HTP-1 / 2耗尽边界标记交叉位点的证据。在htp-1突变体中,Diakinesis二价缺乏正常的不对称特征,在减数分裂分裂期间,姐妹染色单体的内聚力过早丧失。我们得出的结论是,HTP-1是连接交叉与晚期前期二价分化的机制的核心,并定义了在减数分裂II之前内聚力将受到保护的域。此外,我们讨论了在响应交叉而去除HTP-1 / 2的模式与交叉干扰现象之间的相似之处。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号