Fig. 7

Transcriptional activity of zebrafish Gli1, Gli2, and Gli3 in C17 neuronal cells. (A–D) pcDNA constructs encoding zebrafish Gli1, Gli2, Gli3, and the yot^ty119 Gli2-dominant repressor (Gli2-DR) (Karlstrom et al., 2003) proteins were transfected into C17 cells along with a luciferase reporter gene under the transcriptional control of eight Gli1 binding sites (Sasaki et al., 1997). (A) In the absence of Shh, Gli1 (but not Gli2 or Gli3) can activate the reporter in a dose-dependent manner. (B) Cotransfection of multiple gli constructs in the absence of Shh shows that Gli2, truncated Gli2 proteins encoded by zebrafish you-too mutants, and Gli3 can all repress Gli1-mediated transcriptional activity. (C, D) The same experiments were performed in a cell line stably expressing Shh (Feng et al., 2004). (C) In the presence of Shh, Gli1 activator function is largely unaltered, and Gli2 and Gli3 do not activate the reporter construct. (D) In the presence of Shh, Gli3 expression enhances rather than represses Gli1-mediated reporter gene expression.