Fig. 4. Deletion of the HBS1 site in the 1.1 kb 3' Wnt1 enhancer element results in ectopic expression of transgenes within the telencephalon. (A-C) Whole-mount histochemical analysis of ß-galactosidase expression in Wnt1-lacZ-HBS1 transgenic mice at 8.75 (A), 10.5 (B) and 16.5 dpc (C). Ectopic expression was highest in the dorsomedial telencephalon (A-C, red arrowheads) with a gradient of expression diminishing ventrally (C). Ectopic expression was also noted in the rostral diencephalon (B,C). Expression of the transgene was relatively weak in the endogenous Wnt1 expression domain, including the roof plate and mid-hindbrain junction compared with previous analyses of the full-length Wnt1 1.1 kb enhancer (Iler et al., 1995; Rowitch et al., 1998) (B, red arrow). (D) Summary of the wild-type endogenous Wnt1 expression pattern (blue) and ectopic telencephalic expression (red), as observed in Wnt1-Tg and Emx2^–/– transgenic mice. (E-H) Representative results of in situ hybridization analysis of coronal sections from 12.5 dpc control (n=4) (E,F) and Wnt1-Tg (n=4) (G,H) telencephalon demonstrated a striking gradient of ectopic Wnt1 expression in the cortical hem and cortical ventricular zone of the transgenic (G,H) mice in a pattern recapitulating that of endogenous Emx2 (E). mes, mesencephalon; di, diencephalon; tel, telencephalon; rp, roof plate of neural tube; r1, rhombomere 1; hem, cortical hem; cpp, choroid plexus primordium; ncx, neocortical ventricular zone.

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