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FIRM SIGNED

Form and Function of the Mitochondrial Retrograde Response

Total Cost €

0

EC-Contrib. €

0

Partnership

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 FIRM project word cloud

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

microdomains    interrogate    benefit    nuclear    mechanism    molecular    escaped    exploited    cytosolic    axis    metabolic    uncontrolled    deficiencies    sensors    elucidating    ca2    remodelled    intermediates    stressed    metabolism    resistance    treatment    cells    crosstalk    rapid    directional    species    sustain    communication    mito    validating    experimental    trafficking    energy    biogenesis    molecules    regulation    cytoprotective    reprogramming    expedite    ros    unveiling    protocols    hypothesise    autophagy    induce    core    stands    defective    communicate    mitochondria    cell    ranging    retro    capitalizes    meet    reactive    therapeutic    environment    bi    determinant    uncharacterized    cholesterol    describing    exerted    steroids    dysregulated    form    generating    abnormal    diagnostic    mechanistic    domains    substrates    oncogenic    mitochondrial    mrr    expertise    function    signalling    proliferative    nucleus    synthesis    demonstrated    counteract    effectors    oxygen    retrograde    modulate    preventive    plan    cellular    enriched    anterograde    unveil   

Project "FIRM" data sheet

The following table provides information about the project.

Coordinator
THE ROYAL VETERINARY COLLEGE 

Organization address
address: ROYAL COLLEGE STREET
city: LONDON
postcode: NW1 OTU
website: www.rvc.ac.uk

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 1˙450˙060 €
 EC max contribution 1˙450˙060 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-COG
 Funding Scheme ERC-COG
 Starting year 2019
 Duration (year-month-day) from 2019-04-01   to  2024-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE ROYAL VETERINARY COLLEGE UK (LONDON) coordinator 1˙450˙060.00

Map

 Project objective

The molecular communication between mitochondria and nucleus is an integrated bi-directional crosstalk - anterograde (nucleus to mitochondria) and retrograde (mitochondria to nucleus) signalling pathways. The mitochondrial retrograde response (MRR) is driven by defective mitochondrial function, which increases cytosolic reactive oxygen species (ROS) and Ca2. Metabolic reprogramming is a key feature in highly proliferative cells to meet the energy needs for rapid growth by generating substrates for cellular biogenesis. In these mitochondria retro-communicate with the nucleus to induce wide-ranging cytoprotective effects exploited to develop resistance against treatment and sustain uncontrolled growth. Recently, the mitochondrial management of cholesterol-derived intermediates for the synthesis of steroids has been demonstrated as a determinant in the oncogenic reprogramming of cellular environment. We hypothesise that cholesterol-enriched domains facilitate the communication between remodelled mitochondria and nucleus to expedite MRR. This mechanism may be exploited during abnormal cell growth in which cholesterol metabolism and associated molecules are increased. This application capitalizes on expertise in cell signalling and metabolism to interrogate core pathways and unveil molecular sensors and effectors that define form and function of the MRR by: I. Elucidating the mechanism of metabolic regulation of MRR, describing the role exerted by cholesterol trafficking; II. Unveiling microdomains for mito-nuclear communication established by remodelled, autophagy escaped, mitochondria; III. Validating protocols to modulate and target MRR for diagnostic and therapeutic benefit; The experimental plan will (i) define a molecular signalling axis that currently stands uncharacterized, (ii) provide mechanistic knowledge for preventive, and (iii) therapeutic applications to counteract deficiencies associated with stressed, dysregulated mitochondria.

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