Fig. 9

Pax7 function is required for skeletal muscle repair in adult zebrafish. (A) DNA lesions for pax7a alleles (oz19, oz23) and the pax7b (oz32) allele. Mutant allele sequence is shown below the wild-type sequence. Red letters and dashes indicate the lesion as well as single nucleotide changes near the CRISPR-induced frameshifting mutation. (B) CRISPR-induced frameshifting mutations in exon 2 of pax7a and pax7b cause truncations in Pax7a and Pax7b proteins, respectively, that eliminate much of the first conserved paired domain (Pax), the entire homeodomain (Hom), and the second Pax domain. The pax7a^oz19 and pax7a^oz23 alleles encode the first 91 of 507 amino acids of the Pax7a protein, as well as an additional 26 and 22 aberrant amino acids, respectively. The pax7b^oz32 allele encodes the first 81 of 510 amino acids of the Pax7b protein, as well as an additional 19 aberrant amino acids. (C-C'') pax7a+/-; pax7b+/- doubly heterozygous sibling controls show normal muscle repair at 4 dpi, indicated by expression of newly-forming myofiber markers, MyHC (A4.1025) and Rbfox1l. (D-D'') In contrast, pax7a-/-; pax7b-/- double homozygous mutants are severely deficient in newly-forming myofibers at 4 dpi, indicated by the near absence of MyHC (A4.1025) and Rbfox1l expression within the injury site. The pax7a^oz23 and pax7b^oz32 alleles were used in these experiments. Scale bar in all panels is 75 µm.