MITOSIGAGE

Mitochondrial crosstalk signalling in the regulation of ageing

 Coordinatore UNIVERSIDAD PABLO DE OLAVIDE 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Spain [ES]
 Totale costo 1˙424˙640 €
 EC contributo 1˙424˙640 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2011-StG_20101109
 Funding Scheme ERC-SG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-06-01   -   2017-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSIDAD PABLO DE OLAVIDE

 Organization address address: Carretera de Utrera Km1
city: SEVILLA
postcode: 41013

contact info
Titolo: Dr.
Nome: Marta
Cognome: Artal Sanz
Email: send email
Telefono: +34 954977911
Fax: +34 954349376

ES (SEVILLA) hostInstitution 1˙424˙640.00
2    UNIVERSIDAD PABLO DE OLAVIDE

 Organization address address: Carretera de Utrera Km1
city: SEVILLA
postcode: 41013

contact info
Titolo: Ms.
Nome: Marta
Cognome: Mercado
Email: send email
Telefono: +34 954349872

ES (SEVILLA) hostInstitution 1˙424˙640.00

Mappa


 Word cloud

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wild    biogenesis    screens    ageing    cellular    defective    molecular    iis    related    signalling    metabolism    animals    regulating    mutants    genetic    mitochondrial    prohibitins    phb    genome    pathway    adjustments    pathways    metabolic    elegans   

 Obiettivo del progetto (Objective)

'Mitochondrial defects are associated with aging and age-related pathology, but the molecular mechanisms regulating mitochondrial function during ageing are poorly understood. The most relevant genetic pathway regulating ageing is the insulin/IGF-1 signalling (IIS) pathway. The mitochondrial prohibitin (PHB) complex influences cellular metabolism and mitochondrial biogenesis, affecting ageing in opposite ways in wild-type animals and IIS-defective C. elegans mutants. The aim of the proposed research programme is to shed light on the intricate communication between mitochondria and cell-signalling networks in the regulation of ageing. Our specific objectives are: 1-Elucidate the cellular signalling pathways involved in the metabolic responses to mitochondrial dysfunction upon PHB depletion in wild type animals and IIS-defective mutants, using genome-wide RNAi screens, 2-Conduct a comprehensive metabolic profiling of wild type and IIS mutants in the presence and absence of prohibitins and 3-Identify genetic suppressors of prohibitins by performing forward genetic suppressor screens. As an ultimate goal, genes discovered in C. elegans will be tested in vertebrate assays for a conserved role in ageing. We will implement an interdisciplinary approach that combines the genetic power of C. elegans with state-of-the-art metabolomic approaches as well as automated sorting and optical imaging technologies to monitor fat content and mitochondrial biogenesis, in a genome-wide scale, in vivo. The fine-tuning of cellular metabolism, by integration of diverse signalling inputs is the molecular basis of longevity. This project represents a truly integrative and innovative approach to identify cellular signalling pathways involved in mediating lifespan-extending metabolism adjustments, and what these metabolic adjustments entail. These studies will provide fundamental insights to understand the ageing process and to combat ageing-related diseases.'

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