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Fig. 6. Cell-autonomous activation of the MAPK pathway is required for OLIG2 induction by SHH. (A) Cultured neuroepithelial cells from E13.5 mouse embryos were infected with a control retrovirus (pBird) encoding GFP alone (a,b,c,d) or a retrovirus encoding GFP and a constitutively active form of RAS (pBird-Ras^V12) (e,f,g,h). Cells were then cultured for 48 hours in the presence of SHHAg. At DIV3, the cultures were assayed for OLIG2 immunoreactivity (c,g) and labelled with Hoechst dye (a,e). In control virus-infected cultures (a,b,c,d) there were no OLIG2-positive cells. However, in activated RAS virus-infected cultures, SHHAg induced OLIG2 expression in a subset of GFP-positive cells (e,f,g,h). (B) The number of OLIG2- and GFP-positive cells was counted and is presented as the percentage of all GFP-positive cells. In RAS virus-infected cultures in the presence of SHHAg, 17.0±1.3% of GFP-positive cells expressed OLIG2. No OLIG2-positive cells were induced by either in the absence of active MAPK (added U0126), or in the absence of SHHAg (added cyclopamine). In all cultures PD173074 was added to block MAPK activation via FGFR.

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