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Form and Function of the Mitochondrial Retrograde Response

Total Cost €


EC-Contrib. €






 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.

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

Project "FIRM" data sheet

The following table provides information about the project.


Organization address
city: LONDON
postcode: NW1 OTU

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


Take a look of project's partnership.

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


 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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The information about "FIRM" are provided by the European Opendata Portal: CORDIS opendata.

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