MKK7 inhibits myelin gene expression in a c-Jun–dependent way. (A) Western blot showing that MKK7, presumably by activating JNK, inhibits Krox-20–induced myelin protein expression. The cells were coinfected with adenoviruses expressing the constructs indicated. (B) Western blot of cells infected with adenoviruses expressing control LacZ or activated MKK7 to activate JNK. Note that periaxin induced by 2 d of exposure to 1 mM of db-cAMP in LacZ control cells is inhibited by MKK7 expression. (C–F) MKK7 activates c-Jun even in the presence of Krox-20. C and E show that Krox-20 coinfected with a control LacZ-expressing adenovirus suppresses c-Jun levels. D and F show that when Krox-20 is coexpressed with MKK7, high c-Jun levels are maintained. (G) MKK7-mediated suppression of myelin gene expression depends on c-Jun. In normal cells (cJun con), Krox-20–induced periaxin expression (K20/LacZ) is suppressed by MKK7 (K20/MKK7). This suppression does not occur when this experiment is repeated in cells without c-Jun (cJun null). Error bars show one standard deviation of the mean. (H–K) Reactivation of JNK/c-Jun in Krox-20–expressing cells that already synthesize P₀ abolishes P₀ protein expression. Retrovirally infected cells already expressing Krox-20 and P₀ were infected with either LacZ control (H and I) or MKK7-expressing (J and K) adenoviruses. Cells were labeled with either LacZ and P₀ (H and I) or MKK7 and P₀ (J and K) antibodies. Note down-regulation of P₀ protein in Krox-20–expressing cells infected with MKK7 adenovirus. Bars, 15 μm.