Figure 1.

Abnormal muscle regeneration in Rbm24 knockout mice. (A) Schematic representation of the construction of the UKO mice. We generated UKO mice by breeding Rbm24^loxP/loxP mice with UBC-CreERT2 mice. (B) Schematic showing the generation of Rbm24 conditional alleles and the method of drug administration. Exons 2 and 3 of Rbm24 were flanked by two loxP sites. The loxP sites are indicated by the arrowheads. Rbm24 deletion was induced by injection of tamoxifen intraperitoneally for 5 consecutive days in 8-week-old mice. (C) Western blot analysis of Rbm24 knockout efficiency in skeletal muscle from 8-week-old mice 3 days after tamoxifen treatment, GAPDH was used as a loading control. Two samples from each group were used as representative examples. (D) H&E staining showing the abnormal regeneration of muscle in mice 4 to 6 months after tamoxifen treatment. Regenerated myofibers with centralized nuclei are denoted by arrowheads. Scale bars, 100 µm. (E) Quantification of the regeneration markers using qPCR. The elevated expression of eMHC, cTnT and Mymk indicated the abnormal regeneration of muscle in the UKO mice. Total RNAs were extracted from the skeletal muscle at 6 months after tamoxifen treatment. Data are presented as mean ± SEM, n = 4, *P < 0.05, unpaired t-test. Abbreviations: cTnT: cardiac Troponin T; eMHC: embryonic MHC; Mymk: myomaker; qPCR: quantitative real-time polymerase chain reaction; UKO: UBC-CreERT2, Rbm24^loxP/loxP.