Loss of Myogenin in adult zebrafish resulted in severely reduced myofibre nuclear number, increased myonuclear domain size, and a fivefold increase in mis-positioned muscle stem cells.
Does loss of Myogenin affect adult myofibre growth and muscle stem cell homeostasis in zebrafish?
Myogenin is essential for adult myofibre growth and muscle stem cell homeostasis, influencing the MuSC:niche relationship beyond myocyte fusion.
Growth and maintenance of skeletal muscle fibres depend on coordinated activation and return to quiescence of resident muscle stem cells (MuSCs). The transcription factor Myogenin (Myog) regulates myocyte fusion during development, but its role in adult myogenesis remains unclear. In contrast to mice, myog -/- zebrafish are viable, but have hypotrophic muscles. By isolating adult myofibres with associated MuSCs, we found that myog -/- myofibres have severely reduced nuclear number, but increased myonuclear domain size. Expression of fusogenic genes is decreased, Pax7 upregulated, MuSCs are fivefold more numerous and mis-positioned throughout the length of myog -/- myofibres instead of localising at myofibre ends as in wild-type. Loss of Myog dysregulates mTORC1 signalling, resulting in an ‘alerted’ state of MuSCs, which display precocious activation and faster cell cycle entry ex vivo, concomitant with myod upregulation. Thus, beyond controlling myocyte fusion, Myog influences the MuSC:niche relationship, demonstrating a multi-level contribution to muscle homeostasis throughout life.
Ganassi et al. (Thu,) conducted a other in Myogenin deficiency. myog-/- mutation vs. myogkg125/+ heterozygous siblings was evaluated on Myofibre nuclear number and muscle stem cell (MuSC) count. Loss of Myogenin in adult zebrafish resulted in severely reduced myofibre nuclear number, increased myonuclear domain size, and a fivefold increase in mis-positioned muscle stem cells.
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