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EndoMitTalk SIGNED

Endolysosomal-mitochondria crosstalk in cell and organism homeostasis

Total Cost €


EC-Contrib. €






Project "EndoMitTalk" data sheet

The following table provides information about the project.


Organization address
city: MADRID
postcode: 28049

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 Spain [ES]
 Total cost 1˙498˙625 €
 EC max contribution 1˙498˙625 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-STG
 Funding Scheme ERC-STG
 Starting year 2017
 Duration (year-month-day) from 2017-03-01   to  2022-02-28


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSIDAD AUTONOMA DE MADRID ES (MADRID) coordinator 1˙498˙625.00


 Project objective

For many years, mitochondria were viewed as semiautonomous organelles, required only for cellular energetics. This view has been displaced by the concept that mitochondria are fully integrated into the life of the cell and that mitochondrial function and stress response rapidly affect other organelles, and even other tissues. A recent discovery from my lab demonstrated that mitochondrial metabolism regulates lysosomal degradation (Cell Metabolism, 2015), thus opening the way to investigate the mechanism behind communication between these organelles and its consequences for homeostasis. With this proposal, we want to assess how mitochondrial crosstalk with endolysosomal compartment controls cellular homeostasis and how mitochondrial dysfunction in certain tissues may account for systemic effects on the rest of the organism. EndoMitTalk will deliver significant breakthroughs on (1) the molecular mediators of endolysosomal-mitochondria communication, and how deregulation of this crosstalk alters cellular (2), and organism homeostasis (3). Our central goals are: 1a,b. To identify metabolic and physical connections mediating endolysosomal-mitochondria crosstalk; 2a. To decode the consequences of altered interorganelle communication in cellular homeostasis 2b. To study the therapeutic potential of improving lysosomal function in respiration-deficient cells; 3a. To assess how unresolved organelle dysfunction and metabolic stresses exclusively in immune cells affects organism homeostasis and lifespan. 3b. To decipher the molecular mediators by which organelle dysfunction in T cells contributes to age-associated diseases, with special focus in cardiorenal and metabolic syndromes. In sum, EndoMitTalk puts forward an ambitious and multidisciplinary but feasible program with the wide purpose of understanding and improving clinical interventions in mitochondrial diseases and age-related pathologies.


year authors and title journal last update
List of publications.
2018 Gabriela Desdín-Micó, Gonzalo Soto-Heredero, María Mittelbrunn
Mitochondrial activity in T cells
published pages: 51-57, ISSN: 1567-7249, DOI: 10.1016/j.mito.2017.10.006
Mitochondrion 41 2019-10-08
2017 Gonzalo Soto-Heredero, Francesc Baixauli, María Mittelbrunn
Interorganelle Communication between Mitochondria and the Endolysosomal System
published pages: , ISSN: 2296-634X, DOI: 10.3389/fcell.2017.00095
Frontiers in Cell and Developmental Biology 5 2019-05-27

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