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. 2021 Mar 8;6(5):e143465. doi: 10.1172/jci.insight.143465

Figure 5. CUG960 mice exhibit strong and reversible DM1-associated splicing defects.

Figure 5

Representative RT-PCRs with quantification showing strong reversion to fetal splicing patterns for Sorbs1 exon 25, Spag9 exon 31, Tnnt2 exons 4 and 5, and the Mef2d β-exon in atria and ventricles of CUG960 +dox mice in comparison with MHCrtTA +dox controls. Splicing defects are completely rescued in CUG960 mice after dox withdrawal. n = 4 animals per group. Data represent the mean ± SD. DM1, myotonic dystrophy type 1; PN0, postnatal day 0 heart; Ad, adult heart ventricle; dox, doxycycline.