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. 2002 Nov 11;159(3):419–429. doi: 10.1083/jcb.200206020

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Copyright © 2002, The Rockefeller University Press

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Figure 7. — Exogenous MyoD rescues the differentiation defect in cells expressing the mutant DMPK 3′-UTR RNA. (A) GFP+mut 3′-UTR pool cells infected with a retrovirus that expresses MyoD regain the ability to form myotubes (stained red by immunofluorescent staining of MHC) as effectively as infected control C2C12 and GFP+wt 3′-UTR pool cultures. Nuclei are stained blue with DAPI. (B) Western blotting shows increased expression of MyoD protein in proliferating cells infected with the MyoD retrovirus. The graph shows relative MyoD levels (normalized to dynein) in infected and uninfected cells. Similar results were seen in three separate infections. (C) Analysis of myogenin protein expression in infected and uninfected cells cultured in differentiation media shows that exogenous MyoD expression corrects the defect in myogenin up-regulation in GFP+mut 3′-UTR pool cells.

Figure 7. — Exogenous MyoD rescues the differentiation defect in cells expressing the mutant DMPK 3′-UTR RNA. (A) GFP+mut 3′-UTR pool cells infected with a retrovirus that expresses MyoD regain the ability to form myotubes (stained red by immunofluorescent staining of MHC) as effectively as infected control C2C12 and GFP+wt 3′-UTR pool cultures. Nuclei are stained blue with DAPI. (B) Western blotting shows increased expression of MyoD protein in proliferating cells infected with the MyoD retrovirus. The graph shows relative MyoD levels (normalized to dynein) in infected and uninfected cells. Similar results were seen in three separate infections. (C) Analysis of myogenin protein expression in infected and uninfected cells cultured in differentiation media shows that exogenous MyoD expression corrects the defect in myogenin up-regulation in GFP+mut 3′-UTR pool cells.