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<italic toggle='yes'>dmd</italic> mutants do not respond to endurance neuromuscular electrical stimulation (eNMES) in the same manner as WT siblings and heme oxygenase is required for eNMES-mediated improvement.RNAseq analysis was performed at 7 days post-fertilization (dpf) in WT siblings and dmd mutants that completed eNMES training, and their expression patterns were compared with their respective controls. (A1) Volcano plot showing significantly and biologically upregulated (blue dots) and downregulated (red dots) genes in WT siblings that completed eNMES versus those that did not. (A2) Volcano plot showing significantly and biologically upregulated (blue dots) and downregulated (red dogs) genes in dmd mutants that completed eNMES versus those that did not. (A3–A4) Summary of differentially expressed genes in WT siblings (A3) and dmd mutants (A4). WT siblings had 932 differentially expressed genes compared to 123 differentially expressed genes in dmd mutants, suggesting that dmd muscle responds differently to eNMES and the genes responsible for eliciting beneficial effects on muscle structure and function are different. (B) hmox1a expression was increased with eNMES in both WT and dmd mutants. (C1) Whereas eNMES significantly reduces the percentage of segments with dystrophy, dmd mutants injected with morpholinos against hmox1a do not show improvement with eNMES. (C2) Representative images of larvae showing that hmox1a is necessary for eNMES-mediated improvement of dmd muscle.
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