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

Figure 1.

Figure 1.

Figure 1.

Figure 1.

The myogenic machinery downstream of myogenin is functional in cells expressing the mutant DMPK 3′-UTR. (A) The temporal progression of major events in the C2C12 differentiation pathway. Cells proliferating in growth media express MyoD and Myf5. When cultured in differentiation media lacking growth factors, cells initiate myogenin expression, exit the cell cycle, turn on muscle-specific structural genes, such as MHC, and fuse into myotubes. (B) Uninfected GFP+mut 3′-UTR pool (mut 3′-UTR) cells show a differentiation defect, and do not fuse into myotubes (stained red by immunofluorescent staining of MHC) as effectively as GFP+wt 3′-UTR pool (wt 3′-UTR) and control C2C12 cells. However, GFP+mut 3′-UTR pool cells infected with a retrovirus that produces myogenin are capable of forming thick myotubes similar to those formed in GFP+wt 3′-UTR pool and C2C12 cells. Infection with a control retrovirus that expresses LacZ has no effect on the differentiation phenotype. Nuclei are stained blue with DAPI. (C) Western blot analysis of cultures in growth media shows exogenous myogenin expression only in cells infected with the myogenin retrovirus (+myg). These blots were also probed for dynein, which serves as a loading control.