(A) Schema of experimental paradigm. The MGE is dissected from 250-μm thick vibratome sections of Six3Cre;Smof/+;ZEG controls (B-D), or Six3Cre;Smof/f;ZEG mutants (E-G). Cells are dissociated, and then plated on a feeder culture of neonatal cortex. Although some Cre+ progenitors fail to activate the GFP reporter (), in this paradigm the β-Gal+ population will primarily be composed of cells derived from Cre-negative (GFP-negative) progenitors (). After 13 days the expression of SST (blue signal pseudocolored from Cy5 in C, D, F, G) by β-Gal+ cells (red) is assessed (arrowheads). (H) Counts of colabeling for β-Gal and SST reveals a two-fold increase of colabeled cells from the mutant MGE (t-test, N=3), suggesting that a cell non-autonomous effect of the Six3Cre;Smof/f mutant results in overproduction of SST+ cells from the mutant MGE. (I, J, K) mRNA in situ hybridization for the SHH signaling targets Gli1, Ptch1, and Nkx6.2 in Cre-negative control E14.5 embryos are enriched in the dorsal-most region of the MGE. (I’, J’, K’) In sections from Six3Cre;Smof/f mutants, these transcripts are expanded into ventral regions of the MGE (black arrows). Lack of co-labeling for Cre and either PTCH1 or Nkx6.2 () strongly suggests that this expansion is a cell non-autonomous effect. Scale bar = 25 μm in (B) and applies to (C-G). Scale bar = 200 μm in (I) and applies to (I’-K’).