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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.

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

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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