• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Atm Inactivation Results in Aberrant Telomere Clustering during Meiotic Prophase
【24h】

Atm Inactivation Results in Aberrant Telomere Clustering during Meiotic Prophase

机译：Atm失活导致减数分裂前期异常端粒聚集。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm ?/? mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a cluster during the leptotene/zygotene transition (bouquet arrangement). Since the ATM protein has been implicated in telomere metabolism of somatic cells, we have set out to investigate the effects of Atm inactivation on meiotic telomere behavior. Fluorescent in situ hybridization and synaptonemal complex (SC) immunostaining of structurally preserved spermatocytes I revealed that telomere clustering occurs aberrantly inAtm ?/? mice. Numerous spermatocytes ofAtm ?/? mice displayed locally accumulated telomeres with stretches of SC near the clustered chromosome ends. This contrasted with spermatogenesis of normal mice, where only a few leptotene/zygotene spermatocytes I with clustered telomeres were detected. Pachytene nuclei, which were much more abundant in normal mice, displayed telomeres scattered over the nuclear periphery. It appears that the timing and occurrence of chromosome polarization is altered in Atm ?/? mice. When we examined telomere-nuclear matrix interactions in spermatocytes I, a significant difference was observed in the ratio of soluble versus matrix-associated telomeric DNA sequences between meiocytes ofAtm ?/? and control mice. We propose that the severe disruption of spermatogenesis during early prophase I in the absence of functional Atm may be partly due to altered interactions of telomeres with the nuclear matrix and distorted meiotic telomere clustering.
机译：AT（共济失调毛细血管扩张）个体经常表现出性腺萎缩， Atm ？/？小鼠由于减数分裂I的前期停滞而表现出生精功能衰竭。染色体运动发生在减数分裂前期，端粒聚集在核膜上，在瘦素/合子转变（花束排列）过程中暂时形成簇。由于ATM蛋白已经参与了体细胞端粒的代谢，因此我们着手研究 Atm 失活对减数分裂端粒行为的影响。荧光原位杂交和结构保留的精母细胞的突触复合物（SC）免疫染色我发现端粒聚集在 Atm ？/？小鼠中异常发生。 Atm ？/？小鼠的许多精母细胞显示出局部聚集的端粒，在簇状染色体末端附近有一段SC延伸。这与正常小鼠的精子生成相反，在正常小鼠中，仅检测到少数具有簇状端粒的瘦素/合子精子细胞I。在正常小鼠中丰富得多的粗线虫核显示出散布在核外围的端粒。看来， Atm ？/？小鼠的染色体极化发生的时间和发生方式发生了改变。当我们检查精子细胞I中端粒-核基质的相互作用时，在 Atm ？/？的减数分裂细胞之间可溶性与基质相关的端粒DNA序列的比率上发现了显着差异。和对照小鼠。我们提出，在没有功能性 Atm 的情况下，前期I期早期精子发生的严重破坏可能部分归因于端粒与核基质相互作用的改变和减数分裂的端粒聚集。

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