Fig. 2.

Ablation of SelK impairs skeletal muscle regeneration. (A) A schematic illustration of the knockout of SelK using CRISPR/Cas-mediated genome engineering. (B) Western blotting analysis of SelK protein levels in the TA muscle of wild-type (Ctrl) mice and SelK KO mice at 5 d postinjury (N = 3). (C) Average overall body weight of adult wild-type mice and SelK KO mice (N = 5). (D) Relative uninjured TA muscle wet weight of adult wild-type and SelK KO mice (N = 5). (E) Immunohistochemistry analysis of SCs markers (Pax7 and MyoG) and SelK in the TA muscle of SelK KO mice at 5 d postinjury (N = 3). Scale bar = 50 μm. (F) H&E staining of TA muscle in adult Ctrl and SelK KO mice at 0, 3, 5 and 7 d postinjury (N = 3). Scale bar = 50 μm. (G) Rate of myofibers containing two or more centrally located nuclei per field and (H) the average cross-sectional area (CSA) of myofibers calculated from TA muscle of Ctrl and SelK KO mice at 5 d postinjury (N = 3). (I) Distribution of regenerative myofiber CSAs of Ctrl and SelK KO mice at 5 d postinjury (N = 3). (J) Immunofluorescence staining of MyHC (green) in TA muscles of Ctrl and SelK KO mice at 5 d postinjury (N = 3) and (K) the percentage of MyHC-positive (MyHC⁺) fibers in TA muscle of Ctrl and SelK KO mice at 5 d postinjury. Nuclei were labelled using DAPI staining. Scale bar = 50 μm. The results are presented as means ± S.D. *p < 0.05, **p < 0.005, values significantly different from the corresponding control by unpaired t-test. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)