Fig. 3. Normal brain development in hEGFR^KI/KI mice. Dorsal view of the brains of control (A) and hEGFR^KI/KI mice (B) isolated 3 months after birth. Histological sections through the frontal cortex (C,E) and hippocampus (D,F) of control (C,D) and hEGFR^KI/KI (E,F) brains showing normal architecture and morphology. (G,H) Sections of Egfr^-/- brains show neuronal degeneration in the cortex (G), starting around postnatal day 5, and groups of ectopic neurones (arrows) in the white matter of the hippocampus (H, arrows) (Sibilia et al., 1998). (C-H) Sections are stained with Haematoxylin and Eosin. (I) Cumulative cell number of Egfr^+/+, hEGFR^KI/+, hEGFR^KI/KI, hEGFR^KI/KI GFAP-Cre and Egfr^-/- primary cortical astrocytes isolated from newborn brains showing that hEGFR^KI/KI astrocytes display a normal proliferation capacity. Removal of the hEGFR^KI allele in astrocytes of hEGFR^KI/KI GFAP-cre mice results in severe proliferation defects as observed in Egfr^-/- astrocytes. (J) Southern blot analysis of genomic DNA isolated from astrocytes shown in I and hybridised with the probe shown in Fig. 1A. The bands corresponding to the different alleles are indicated. EGFR: hEGFR^KI allele after Cre-mediated deletion.