...
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >elF4A controls germline stem cell self-renewal by directly inhibiting BAM function in the Drosophila ovary
【24h】

elF4A controls germline stem cell self-renewal by directly inhibiting BAM function in the Drosophila ovary

机译:elF4A通过直接抑制果蝇卵巢中的BAM功能来控制种系干细胞的自我更新

获取原文
获取原文并翻译 | 示例
           

摘要

Stem cell self-renewal is controlled by concerted actions of extrinsic niche signals and intrinsic factors in a variety of systems. Drosophila ovarian germline stem cells (GSCs) have been one of the most productive systems for identifying the factors controlling self-renewal. The differentiation factor BAM is necessary and sufficient for GSC differentiation, but it still remains expressed in GSCs at low levels. However, it is unclear how its function is repressed in GSCs to maintain self-renewal. Here, we report the identification of the translation initiation factor elF4A for its essential role in self-renewal by directly inactivating BAM function. elF4A can physically interact with BAM in Drosophila S2 cells and yeast cells. elF4A exhibits dosage-specific interactions with bam in the regulation of GSC differentiation. It is required intrinsically for controlling GSC self-renewal and proliferation but not survival. In addition, it is required for maintaining E-cadherin expression but not BMP signaling activity. Furthermore, BAM and BGCN together repress translation of E-cadherin through its 3' UTR in S2 cells. Therefore, we propose that BAM functions as a translation repressor by interfering with translation initiation and elF4A maintains self-renewal by inhibiting BAM function and promoting E-cadherin expression.
机译:干细胞的自我更新受到外部利基信号和各种系统内在因素共同作用的控制。果蝇卵巢种系干细胞(GSC)已成为确定控制自我更新的因素的最有生产力的系统之一。分化因子BAM是GSC分化所必需和充分的,但仍在GSC中低水平表达。但是,目前尚不清楚在GSC中如何抑制其功能以维持自我更新。在这里,我们报告通过直接使BAM功能失活来鉴定翻译起始因子elF4A在自我更新中的重要作用。 eIF4A可以与果蝇S2细胞和酵母细胞中的BAM物理相互作用。 eIF4A在调节GSC分化中表现出与bam的剂量特异性相互作用。它本质上是控制GSC自我更新和增殖所必需的,而不是生存所必需的。另外,需要维持E-钙粘着蛋白表达而不是BMP信号传导活性。此外,BAM和BGCN一起通过S2细胞中的3'UTR抑制E-cadherin的翻译。因此,我们建议BAM通过干扰翻译起始来充当翻译阻遏物,而elF4A通过抑制BAM功能并促进E-钙粘蛋白表达来维持自我更新。

著录项

  • 来源
  • 作者单位

    stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110;

    stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110;

    stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110 Institute of Biophysics, Chinese Academy of Sciences, 15 Da Tun Road, Beijing 100101, China;

    stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110 University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, KS 66160;

  • 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

    BGCN; e-cadherin; niche; translation;

    机译:BGCN;电子钙粘蛋白利基翻译;

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