MITRAC

Mitochondrial translational regulation coupled to respiratory chain assembly and protein import

 Coordinatore UNIVERSITAETSMEDIZIN GOETTINGEN - GEORG-AUGUST-UNIVERSITAET GOETTINGEN - STIFTUNG OEFFENTLICHEN RECHTS 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 2˙283˙816 €
 EC contributo 2˙283˙816 €
 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-2013-ADG
 Funding Scheme ERC-AG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-02-01   -   2019-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAETSMEDIZIN GOETTINGEN - GEORG-AUGUST-UNIVERSITAET GOETTINGEN - STIFTUNG OEFFENTLICHEN RECHTS

 Organization address address: Robert-Koch-Strasse 40
city: GOETTINGEN
postcode: 37075

contact info
Titolo: Mrs.
Nome: Christiane
Cognome: Hennecke
Email: send email
Telefono: 49551398770
Fax: 495514000000

DE (GOETTINGEN) hostInstitution 2˙283˙817.00
2    UNIVERSITAETSMEDIZIN GOETTINGEN - GEORG-AUGUST-UNIVERSITAET GOETTINGEN - STIFTUNG OEFFENTLICHEN RECHTS

 Organization address address: Robert-Koch-Strasse 40
city: GOETTINGEN
postcode: 37075

contact info
Titolo: Prof.
Nome: Peter
Cognome: Rehling
Email: send email
Telefono: 49551395947
Fax: 49551395979

DE (GOETTINGEN) hostInstitution 2˙283˙817.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

translation    mechanisms    membrane    mitochondrial    nuclear    mitochondria    complexes    intermediates    subunits    imported    encoded    protein    human    chain    oxidase    assembly    regulatory    yeast    influx    cytochrome    respiratory   

 Obiettivo del progetto (Objective)

'Mitochondrial respiratory chain complexes assemble from nuclear- and mitochondria-encoded subunits in the inner membrane. To protect cells from accumulating unassembled subunits in the membrane, ROS generation, or damage of mitochondrial integrity, regulatory mechanisms to balance and control the fidelity of the assembly process have evolved, encorporating a retention system enabling the preservation of a select few founding complexes for on-demand assembly. In yeast mitochondria, a feedback mechanism has been identified for the cytochrome oxidase in which assembly-intermediates specifically inactivate translation of the core subunit Cox1. It is controversially debated if similar translation regulating mechanisms exist in human mitochondria. However, our recent findings show that in human mitochondria assembly intermediates of respiratory chain complexes affect translation, nevertheless the underlying sensing and signalling mechanisms as well as the protein components appear to be more complex than in yeast. We aim to understand how this regulatory cycle is established; how does a distinct assembly intermediate of cytochrome oxidase signal the translation system, and how the influx of imported subunits contributes to this process. These goals are conceptually deeply rooted in a comprehensive understanding of the membrane protein complex assembly process and the factors that promote its progression. These objectives are of key importance for understanding the molecular pathology of mitochondrial encephalomyopathies that are frequently due to respiratory chain assembly and quality control malfunction. The aim of our analyses is to provide insight as to how translation can be coupled to the assembly of a membrane protein complex comprised of subunits of dual genetic origin and to decipher mitochondrial translational regulation coupling to the influx of imported nuclear encoded subunits.'

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