Exon skipping has been demonstrated to be a successful strategy for the gene 
therapy of Duchenne muscular dystrophy (DMD): the rational being to convert 
severe Duchenne forms into milder Becker ones. Here, we show the selection of U1 
snRNA-antisense constructs able to confer effective rescue of dystrophin 
synthesis in a Δ44 Duchenne genetic background, through skipping of exon 45; 
moreover, we demonstrate that the resulting dystrophin is able to recover timing 
of myogenic marker expression, to relocalize neuronal nitric oxide synthase 
(nNOS) and to rescue expression of miRNAs previously shown to be sensitive to 
the Dystrophin-nNOS-HDAC2 pathway. Becker mutations display different 
phenotypes, likely depending on whether the shorter protein is able to 
reconstitute the wide range of wild-type functions. Among them, efficient 
assembly of the dystrophin-associated protein complex (DAPC) and nNOS 
localization are important. Comparing different Becker deletions we demonstrate 
the correlation between the ability of the mutant dystrophin to relocalize nNOS 
and the expression levels of two miRNAs, miR-1 and miR29c, known to be involved 
in muscle homeostasis and to be controlled by the Dys-nNOS-HDAC2 pathway.