MECHANISMS OF AP-3 FUNCTION IN VESICLE FORMATION AND GOLGI MATURATION

AP-3 在囊泡形成和高尔基体成熟中的功能机制

基本信息

  • 批准号:
    10226217
  • 负责人:
  • 金额:
    $ 46.65万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2019
  • 资助国家:
    美国
  • 起止时间:
    2019-09-12 至 2023-07-31
  • 项目状态:
    已结题

项目摘要

PROJECT SUMMARY The secretory pathway folds, assembles, and sorts membrane and secreted proteins and targets them to a variety of locations inside and outside the cell. The `Grand Central Station' of the cell is the trans Golgi network (TGN), an incredibly dynamic and complex structure that packages cargo into separate containers and dispatches them to their terminal destinations. The AP-3 trafficking complex sorts cargo from endosomes or the Golgi into containers bound for endolysosomal compartments, bypassing the endosomal multivesicular body and ESCRT pathway. AP-3 is needed for productive assembly of HIV and other viral capsids. Genetic lesions impairing AP-3 function cause multiple diseases, including Hermansky-Pudlak Syndrome type 2 and an epilepsy-like syndrome. Despite its importance, remarkably little is known about the mechanisms of AP-3 function. In this collaborative Project, we exploit published and unpublished genetic, cell biological, and biochemical advances, and employ state of the art imaging approaches, to dissect the mechanisms of AP-3 budding and the consequences of AP-3 function for the overall dynamics of the TGN, in the model organism Saccharomyces cerevisiae. In Aim 1, we build on proteomic surveys, functional genomic surveys, and follow-up analyses, wich identify new candidate AP-3 cofactors including a ubiquitin ligase. We will use these advances to test hypotheses about the assembly, maturation, and dispatch of AP-3 vesicles from the TGN. In Aim 2, we build on preliminary findings showing that disruption of AP-3 activity causes striking and unexpected global perturbations of Golgi architecture. We hypothesize, based on published and unpublished data, that distinct carriers exit the TGN in a programmed, sequential manner, with AP-3 carriers departing early. We will further test this model and dissect the molecular mechanisms though which the sequence of events is programmed. Together, these studies should establish new paradigms for AP-3 vesicle formation and for organelle maturation dynamics in the Golgi-endolysosomal system.
项目总结

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Alexey Jarrell Merz其他文献

Alexey Jarrell Merz的其他文献

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{{ truncateString('Alexey Jarrell Merz', 18)}}的其他基金

MOLECULAR BASIS OF PILUS-MEDIATED GONOCOCCAL ADHESION
菌毛介导的淋球菌粘附的分子基础
  • 批准号:
    10363679
  • 财政年份:
    2021
  • 资助金额:
    $ 46.65万
  • 项目类别:
MECHANISMS OF AP-3 FUNCTION IN VESICLE FORMATION AND GOLGI MATURATION
AP-3 在囊泡形成和高尔基体成熟中的功能机制
  • 批准号:
    10456623
  • 财政年份:
    2019
  • 资助金额:
    $ 46.65万
  • 项目类别:
MECHANISMS OF AP-3 FUNCTION IN VESICLE FORMATION AND GOLGI MATURATION
AP-3 在囊泡形成和高尔基体成熟中的功能机制
  • 批准号:
    9815765
  • 财政年份:
    2019
  • 资助金额:
    $ 46.65万
  • 项目类别:
MECHANISMS OF AP-3 FUNCTION IN VESICLE FORMATION AND GOLGI MATURATION
AP-3 在囊泡形成和高尔基体成熟中的功能机制
  • 批准号:
    10017291
  • 财政年份:
    2019
  • 资助金额:
    $ 46.65万
  • 项目类别:
PROTEIN PHOSPHORYLATION IN YEAST VACUOLE FUSION
酵母液泡融合中的蛋白质磷酸化
  • 批准号:
    8171286
  • 财政年份:
    2010
  • 资助金额:
    $ 46.65万
  • 项目类别:
PROTEIN PHOSPHORYLATION IN YEAST VACUOLE FUSION
酵母液泡融合中的蛋白质磷酸化
  • 批准号:
    7957800
  • 财政年份:
    2009
  • 资助金额:
    $ 46.65万
  • 项目类别:
PROTEIN INTERACTIONS WITH VACUOLE TARGETING MACHINERY
蛋白质与液泡靶向机制的相互作用
  • 批准号:
    7957852
  • 财政年份:
    2009
  • 资助金额:
    $ 46.65万
  • 项目类别:
FLUORESCENCE MICROSCOPY OF PROTEINS INVOLVED IN GOLGI-TO-VACUOLE VESICLE TRAFFIC
参与高尔基体到液泡囊泡运输的蛋白质的荧光显微镜
  • 批准号:
    7723724
  • 财政年份:
    2008
  • 资助金额:
    $ 46.65万
  • 项目类别:
Dynamics of Endomembrane Docking and Fusion
内膜对接和融合的动力学
  • 批准号:
    10386618
  • 财政年份:
    2006
  • 资助金额:
    $ 46.65万
  • 项目类别:
Dynamics of endomembrane docking and fusion
内膜对接和融合的动力学
  • 批准号:
    7368053
  • 财政年份:
    2006
  • 资助金额:
    $ 46.65万
  • 项目类别:

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