A research group led by Assistant Professor Ryo Fujita of the University of Tsukuba Medical School has clarified a part of the mechanism by which skeletal muscle stem cells replicate and amplify themselves.Key research findings for developing long-term amplification methods for skeletal muscle stem cells may be useful in the treatment of sarcopenia and hereditary muscle diseases.

 Muscle (skeletal muscle) has a very high regenerative capacity, and its central role is played by skeletal muscle stem cells in skeletal muscle tissue.Skeletal muscle also plays an important role as a tissue that controls energy metabolism throughout the body.However, due to aging and illness, the ability of skeletal muscle stem cells decreases, which may cause deterioration of muscle mass and quality, and sarcopenia (age-related muscle weakness).To maintain normal skeletal muscle, it is necessary to elucidate the mechanism for maintaining the amplification and properties of skeletal muscle stem cells.

 The research group identified a new molecular mechanism that regulates self-renewal of skeletal muscle stem cells, with the hint that phosphorylation of the molecule involved in protein translation (eIF2α) is strongly induced in self-replicating cells.Phosphorylation of this molecule was generally known to suppress protein translation, but analysis identified a molecule (TACC3) in which protein translation was enhanced.

 This suggests that skeletal muscle stem cells may control self-renewal and amplification of skeletal muscle stem cells by selectively inducing translation of TACC2 while suppressing protein translation of the entire cell through phosphorylation of eIF3α. Was done.

 By elucidating the unique protein translation mechanism of eIF2α and identifying TACC3, long-term in vitro culture of skeletal muscular stem cells, which has been considered difficult until now, has become possible, and aging-related loss of muscle mass and strength (sarcopenia) and It is expected to contribute to the development of treatments for muscular dystrophy and the like.

Paper information:[Development] Satellite cell expansion is mediated by P-eIF2a dependent Tacc3 translation

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