Fig. 6
From: A need for NAD+ in muscle development, homeostasis, and aging
Cellular and molecular mechanisms of amelioration of muscle disease due to NAD+ repletion. (A, B) Model of pathological changes observed in animal models of diseased muscle (A) and the improvement in these disease phenotypes due to provision of dietary NAD+ precursors or NAD+ (B). (C, D) Anterior left, dorsal top, side-mounted, 3 dpf embryos stained with phalloidin to visualize actin. Fiber detachment is readily observed in dag1 morphants (C, white arrowheads), whereas dag1 morphants supplemented with NAD+ display less fiber detachment (D). (E, F) Transmission electron micrographs showing normal muscle ECM (white arrows), disrupted muscle ECM (red arrows), normal sarcomere structure (white arrowheads), and disrupted sarcomere structure (red arrowheads) in a zebrafish model of muscular dystrophy with and without NAD+ supplementation. (E) Dag1-deficient zebrafish. (F) Dag1-deficient zebrafish supplemented with NAD+