首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4
【24h】

Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4

机译:Lte1通过控制纺锤体位置检查点激酶Kin4的定位来促进有丝分裂退出

获取原文
获取原文并翻译 | 示例
           

摘要

For a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from mitosis. The protein kinase Kin4 is a central component of the spindle position checkpoint. Kin4 primarily localizes to the mother cell and associates with spindle pole bodies (SPBs) located in the mother cell to inhibit MEN signaling. In contrast, the kinase does not associate with the SPB in the bud. Thus, only when a MEN bearing SPB leaves the mother cell and the spindle is accurately positioned along the mother-bud axis can MEN signaling occur and cell division proceed. Here, we describe a mechanism ensuring that Kin4 only associates with mother cell-located SPBs. The bud-localized MEN regulator Lte1, whose molecular function has long been unclear, prevents Kin4 that escapes into the bud from associating with SPBs in the daughter cell.
机译:为了使子细胞接收完整的基因组补体,必须将有丝分裂纺锤体准确定位在细胞内。在发芽酵母中,称为纺锤体位置检查点(SPOC)的信号传导系统会监控纺锤体位置并调节有丝分裂出口网络(MEN)的活性,这是一种促进有丝分裂的GTPase信号传导途径。蛋白激酶Kin4是纺锤体位置检查点的重要组成部分。 Kin4主要位于母细胞中,并与位于母细胞中的纺锤极体(SPB)相关联以抑制MEN信号传导。相反,该激酶不与芽中的SPB缔合。因此,只有当带有MEN的SPB离开母细胞并且主轴沿着母芽轴准确定位时,MEN信号才会发生,并且细胞分裂会继续进行。在这里,我们描述一种机制,确保Kin4仅与位于母细胞上的SPB关联。芽定位的MEN调节剂Lte1(其分子功能长期不清楚)可防止逃逸到芽中的Kin4与子细胞中的SPB结合。

著录项

  • 来源
  • 作者单位

    David H. Koch Institute for Integrative Cancer Research and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139;

    Department of Molecular and Cell Biology and QB3, University of California, Berkeley, CA 94720-3200;

    David H. Koch Institute for Integrative Cancer Research and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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