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eIF3-f function in skeletal muscles: To stand at the crossroads of atrophy and hypertrophy

Alfredo Csibi, Lionel A. Tintignac, Marie Pierre Leibovitch and Serge A. Leibovitch

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The control of muscle cell size is a physiological process balanced by a fine tuning between protein synthesis and protein degradation. MAFbx/Atrogin-1 is a muscle specific E3 ubiquitin ligase up regulated during disuse, immobilization, and fasting or systemic diseases such as diabetes, cancer, SIDA and renal failure. This response is necessary to induce a rapid and functional atrophy. To date, the targets of MAFbx/Atrogin-1 in skeletal muscle remain to be identified. We have recently presented evidence that eIF3-f, a regulatory subunit of the eukaryotic translation factor eIF3 is a key target that accounts for MAFbx/Atrogin-1 function in muscle atrophy. More importantly, we showed that eIF3-f act as a “translational enhancer” that increases the efficiency of the structural muscle proteins synthesis leading to both in vitro and in vivo muscle hypertrophy. We propose that eIF3-f subunit, a mTOR/S6K1 scaffolding protein in the IGF-1/Akt/mTOR dependant control of protein translation, is a positive actor essential to the translation of specific mRNAs probably implicated in the muscle hypertrophy. The central role of eIF3-f in both the atrophic and hypertrophic pathways will be discussed in the light of its promising potential in muscle wasting therapy.

Authors

Alfredo Csibi

UMR866 Différenciation Cellulaire et Croissance; Montpellier, France

Lionel A. Tintignac

UMR866 Différenciation Cellulaire et Croissance; Montpellier, France

Marie Pierre Leibovitch

UMR866 Différenciation Cellulaire et Croissance; Montpellier, France

Serge A. Leibovitch

UMR866 Différenciation Cellulaire et Croissance; Montpellier, France

Purchase article for $19

Subscribe to this journal for $129/year