Figure 2.

Loss of Sfpq in Skeletal Muscle Causes Metabolic Myopathy but Not Typical Dystrophic Phenotypes

(A and B) (A) Representative cross-section of H&E-stained TA muscle from 1-month-old male KO and control mice. Scale bars: 100 μm. (B) Representative cross-section of modified Gomori trichrome stained TA muscle from 1-month-old male KO and control mice. Scale bars: 100 μm (left). Representative cross-section of NADH-TR stained TA muscle from 1-month-old male KO and control mice. Scale bars: 100 μm (right).

(C) Percentage distribution of MyHC isoforms I, IIA, and IIB in TA muscle of male KO and control mice (n = 3, totally three sections from three mice in each genotype). Data are presented as mean ± SD. *p < 0.05, **p < 0.01 (Student's t test).

(D) Representative results of WB using an OXPHOS antibody cocktail on TA muscle samples from male KO and control mice. Lamin B1 was used as a loading control. Signal intensities were quantified by densitometry (n = 3). CI, complex I (Ndufb8); CII, complex II (Sdhb); CIII, complex III (Uqcrc2); CIV, complex IV (mt-Co1); and CV, complex V (Atp5a1). Data are presented as mean ± SD. *p < 0.05, **p < 0.01 (Student's or Welch's t test).

(E) Representative periodic acid Schiff staining of GC sections from 1-month-old male KO and control mice. Scale bars: 100 μm.

(F) Glycogen content in GC muscles from 1-month-old male KO and control mice (n = 3). Data are presented as mean ± SD. **p < 0.01 (Student's t test).