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In vitro high resolution reconstitution of autophagosome nucleation and expansion catalyzed byATG9

Total Cost €


EC-Contrib. €






 ATG9_SOLVES_IT project word cloud

Explore the words cloud of the ATG9_SOLVES_IT project. It provides you a very rough idea of what is the project "ATG9_SOLVES_IT" about.

torc1    expand    cargo    transmembrane    nucleation    traffics    functional    aging    nucleate    manipulation    electron    deregulation    acutely    lipids    molecular    assayed    biochemically    dissection    interact    uncover    identification    optogenetic    membrane    proximity    master    survival    functions    mediated    property    tomography    immunity    microscopy    light    tools    reconstituted    lastly    membranes    modulate    homeostasis    correlative    proteins    protein    components    rapid    vesicle    biotinylation    crucially    acid    signaling    endocytic    resolution    autophagosomes    secretory    conserved    lysosomal    mass    ampk    initiating    quantitative    employ    initiates    amino    regulators    reconstitution    energy    regulate    expansion    resident    vesicles    neurodegeneration    form    autophagy    composition    unknown    cancer    disease    generation    atg    atg9    em    spectrometry    translational    selective    cell    proteome    starvation    implicated    cryo    autophagosome    tested    function    therapies    recruitment    vitro    occurs    infection    initiation    accessory   

Project "ATG9_SOLVES_IT" data sheet

The following table provides information about the project.


Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 2˙121˙055 €
 EC max contribution 2˙121˙055 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-ADG
 Funding Scheme ERC-ADG
 Starting year 2018
 Duration (year-month-day) from 2018-07-01   to  2023-06-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Autophagy is a conserved, lysosomal-mediated pathway required for cell homeostasis and survival. It is controlled by the master regulators of energy (AMPK) and growth (TORC1) and mediated by the ATG (autophagy) proteins. Deregulation of autophagy is implicated in cancer, immunity, infection, aging and neurodegeneration. Autophagosomes form and expand using membranes from the secretory and endocytic pathways but how this occurs is not understood. ATG9, the only transmembrane ATG protein traffics through the cell in vesicles, and is essential for rapid initiation and expansion of the membranes which form the autophagosome. Crucially, how ATG9 functions is unknown. I will determine how ATG9 initiates the formation and expansion of the autophagosome by amino acid starvation through a molecular dissection of proteins resident in ATG9 vesicles which modulate the composition and property of the initiating membrane. I will employ high resolution light and electron microscopy to characterize the nucleation of the autophagosome, proximity-specific biotinylation and quantitative Mass Spectrometry to uncover the proteome required for the function of the ATG9, and optogenetic tools to acutely regulate signaling lipids. Lastly, with our tools and knowledge I will develop an in vitro reconstitution system to define at a molecular level how ATG9 vesicle proteins, membranes that interact with ATG9 vesicles, and other accessory ATG components nucleate and form an autophagosome. In vitro reconstitution of autophagosomes will be assayed biochemically, and by correlative light and cryo-EM and cryo-EM tomography, while functional reconstitution of autophagy will be tested by selective cargo recruitment. The development of a reconstituted system and identification proteins and lipids which are key components for autophagosome formation will provide a means to identify a new generation of targets for translational work leading to manipulation of autophagy for disease related therapies.

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