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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.

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

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

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 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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