Figure 2
Recombination in Glast ::Cre;R26R embryos parallels endogenousGLAST (glial high affinity glutamate transporter) expression and the patternobserved in Blbp ::Cre;R26R embryos. (a-q) Wild-type (a-f),Glast::Cre;R26RlacZ (g-m) and Glast::Cre;Z/EG (n-q) embryos immunostainedfor GLAST (a,b,e,f,k,l), BLBP (c-f), phosphorylated histone H3 (PH3) (n,o,q)or GFP (p,q) and X-gal staining (g-j,k',l',m'). Sections in (a-j) aresagittal; (k-q) are coronal. At E9.5, endogenous GLAST (a) and BLBP (c)expression was detected in hindbrain and spinal cord, but not intelencephalon until E10.5 (b,d). Double labeling for GLAST (red) and BLBP(green) in E10.5 CX and GE confirmed that both are upregulated in the samecells (e,f). The onset of Cre recombination matched the spatiotemporalpattern of endogenous GLAST expression, with minimal β-Gal activity in E9.5telencephalon (g,h) but extensive staining by E10.5 (i,j); this patternmatches that previously reported for Blbp::Cre;R26R embryos [8]. Concordance between β Gal activity and GLAST+ RG was consistently observed. At E12.5,GLAST is weak in septum (k'), and recombination in this region was similarlyminimal (k). Conversely, GLAST and recombination are intense in the corticalhem (arrow in (l); higher magnification image of GLAST hem staining in(l')). Further, both Cre mRNA1c) and recombination (m) in the spinal cord matched the dorsoventral gradient of endogenous GLAST in this region (Figure 1r). PH3 and GFP labeling in the E14.5 GE of Glast::Cre;Z/EGembryos showed that mitotic SVZ progenitors were recombined (n-q). (asobserved in Blbp::Cre;R26R embryos [8], establishing that GE SVZprogenitors are RG-derive. Scale bars: 400 μm (a,c,g,i); 200 μm (k); 175 μm (b,d,j); 150 μm (h); 100 μm (m); 40 μm (f,n); 25 μm (l); 20 μm (e,o-q).