The hGFAP promoter fails to drive recombination in fully morphologically differentiated radial glia (RG) of the ventral telencephalon and thalamus. Immunostaining for eGFP (green) (a-c,g,i,j,l,p,q) and GLAST(red) (d-f,h,k,l), X-gal staining for β-gal (m-o) and Cre ISH (r) onhGFAP::Cre;Z/EG (a-l), hGFAP::Cre;R26R (m-o,r) or hGFAP::eGFP (p,q) embryos,at E12.5 (a-l), E14.5 (m,n,p,q), E15.5 (o), and E16.5 (r). Panels (b,c,e,f)show cortex and GE in (a,d) at higher magnification; panels (h,i) showthalamus in (g) at higher magnification, arrows in (g-i) mark identicalspots in all three panels; panels (n,q) show higher magnification images ofcortex and GE in (m,p). In contrast to the Blbp and Glast promoters, thehGFAP promoter is not active in forebrain prior to E12.5 (not shown). ByE12.5, recombination is detected in cortical RG but absent from GE (a-c),thalamus (g,i) and cortical hem (j,l). Importantly, both BLBP (not shown)and GLAST (d-f,h,k,l) are highly expressed in these regions. Moreover, theseunrecombined cells have molecular and morphological properties of fullydifferentiated RG cells (e.g. long radial processes coursing from VZ topia). Even as late as E14.5, few GE RG are recombined (m,n), and significantrecombination is not observed until E15.5 (o) when most RG in the regionhave completed neurogenesis. hGFAP promoter activity itself is not onlydelayed with respect to RG differentiation, but also weak ventrally comparedto its dorsal activity (p,q,r). Scale bars: 300 μm (m,o,r); 200 μm (a,d,p); 100 μm (c,f,g,n,q); 60 μm (b,e,h-l).