Supplementary Figure 5: DHT and E2 independently drive the conversion of cycling SCs into quiescent SCs.

(a–d) The expression of Mib1 (a,c), androgen receptor (Ar, b), and estrogen receptor β (Esr2, d) in TA muscles. Ten-day-old Mib1^WT and Mib1^ΔMF mice were s.c. injected with Veh, DHT, or E2, and TA muscles were isolated 3 days after injection. Both DHT and E2 treatment induced the expression of the target genes Ar and Esr2, respectively, in Mib1^WT and Mib1^ΔMF TA muscles. n = 5 animals for each group; data are mean ± s.d.; two-sample t-test; ^∗P < 0.05. Statistical source data for a–d is provided in Supplementary Table 2. (e–h) IHC staining of Pax7 (e,f), MyoD (g,h) and Ki67 in TA muscles from 10-day-old mice injected with Veh, DHT (e,g) or E2 (f,h). TA muscles were isolated 3 days after injection. Most Pax7⁺ cells were still Ki67⁺ and the number of cycling MyoD⁺ cells was maintained by either DHT or E2 treatment in Mib1^ΔMF TA muscles, while Pax7⁺ cells were Ki67⁻ and the MyoD⁺ cells significantly decreased in Mib1^WT TA muscles. Arrows and arrowheads indicate Ki67⁺ and Ki67⁻ cells, respectively; scale bar, 20 μm. (i,j) Quantification of Pax7 and Ki67 in 10-day-old TA muscles treated with Veh, DHT (i) or E2 (j) as in e,f. n = 3 animals for each group; data are mean ± s.d.; Poisson’s general linear model regression; ^∗P < 0.05; N.S. not significant. Statistical source data for i,j is provided in Supplementary Table 2.