...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Disrupting Vesicular Trafficking at the Endosome Attenuates Transcriptional Activation by Gcn4
【24h】

Disrupting Vesicular Trafficking at the Endosome Attenuates Transcriptional Activation by Gcn4

机译：在内体破坏水泡贩运削弱了Gcn4的转录激活。

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

摘要

The late endosome (MVB) plays a key role in coordinating vesicular transport of proteins between the Golgi complex, vacuole/lysosome, and plasma membrane. We found that deleting multiple genes involved in vesicle fusion at the MVB (class C/D vps mutations) impairs transcriptional activation by Gcn4, a global regulator of amino acid biosynthetic genes, by decreasing the ability of chromatin-bound Gcn4 to stimulate preinitiation complex assembly at the promoter. The functions of hybrid activators with Gal4 or VP16 activation domains are diminished in class D mutants as well, suggesting a broader defect in activation. Class E vps mutations, which impair protein sorting at the MVB, also decrease activation by Gcn4, provided they elicit rapid proteolysis of MVB cargo proteins in the aberrant late endosome. By contrast, specifically impairing endocytic trafficking from the plasma membrane, or vesicular transport to the vacuole, has a smaller effect on Gcn4 function. Thus, it appears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, and not merely the failure to transport cargo properly to the vacuole or downregulate plasma membrane proteins by endocytosis, is required to attenuate substantially transcriptional activation by Gcn4.
机译：晚期内体（MVB）在协调蛋白质在高尔基体，液泡/溶酶体和质膜之间的囊泡运输中起关键作用。我们发现，删除涉及MVB的囊泡融合的多个基因（C / D类 vps 突变）会降低氨基酸染色质的能力，从而削弱Gcn4的转录激活，Gcn4是氨基酸生物合成基因的全球调节者。结合Gcn4以刺激启动子处的预启动复合物组装。在D类突变体中，具有Gal4或VP16激活域的混合激活子的功能也减弱了，这表明激活中存在更广泛的缺陷。 E类 vps 突变会破坏MVB处的蛋白质分选，也会降低Gcn4的激活，前提是它们引起异常晚期内体中MVB货物蛋白的快速蛋白水解。相比之下，特别损害从质膜的内吞运输，或水泡运输到液泡，对Gcn4功能的影响较小。因此，似乎需要通过减弱传递或增强的降解来降低MVB中的货物蛋白，而不仅仅是通过内吞作用不能将货物正确地转运至液泡或下调质膜蛋白，才能实质上减弱Gcn4的转录激活。

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