ZFIN Image: Ganassi et al., 2018, Fig. 8

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Fig. 8

Mutant adult-derived muscle progenitor cells retain fusion deficit ex vivo. a Immunodetection of desmin (green) and MyHC (red) and nuclei (white, Hoechst) in 15 months old myog^kg125 and sibling myog^kg125/+ adult-derived MPCs following 5 days of differentiation. Fusion into multinucleated myofibres occurred only in sib (magnified boxes), coloured arrowheads indicate nuclei of each cell. Representative images, n = 3. b Extent of differentiation (Differentiation index) is comparable between mutant and heterozygous MPCs. c Fusion index showing deficit in fusion of mutant myocytes. d Number of nuclei in fused MyHC⁺ cells is reduced in mutant, χ² test. Three fish per genotype (three technical replicates each). e Schematic of the role of Myogenin during differentiation, fusion and growth of muscle fibres. During myogenesis, committed MPCs leave the cell cycle, begin to elongate and express early muscle-specific genes during terminal differentiation into myocytes. At this stage, Myogenin (MYOG) promotes the expression of myomaker (MYMK), myomixer (MYMX) and jam3b (JAM3B). These fusogenic proteins prompt myocyte fusion to form muscle fibres. In the absence of Myogenin, myocytes undergo terminal differentiation but fail to express Myog-module genes, remain mononucleated and grow less throughout life. Residual myocyte fusion in Myog mutants in the medial region of the somite (bracket) is sustained by Hedgehog (Hh) signalling

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