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Fig. 3. Dorso-ventral patterning in the telencephalon of mice harboring mutations in the distinct DNA-binding domains of Pax6. Micrographs of coronal sections of the lateral telencephalon at embryonic day (E) 14. (A-D) In WT CTX, but not GE, precursors are Ngn2-immunopositive (red), while precursors in the GE, but not the CTX, are Mash1-immunoreactive (green in A-D). Panels from littermate mutant mice are depicted in the right column (A'-D'). Note that Ngn2-immunoreactivity is not detectable in the CTX of mutant mice with a large deletion in the PD (see Fig. 1B), the Pax6^Aey18–/– mice (A') and the functional null allele Pax6^Sey–/– (E'), while it is unaffected in Pax6(5a)–/– (B') and Pax6^4Neu–/– (C'). Conversely, Mash1-immunoreactivity spreads ectopically into the cortex of Pax6^Aey18–/– (A') and Pax6^Sey–/– (D') mice, but is not changed in Pax6(5a)–/– (B') or Pax6^4Neu–/– (C') telencephalon. Thus, the PD of Pax6 seems to be necessary and sufficient to exert patterning of the telencephalon. The dashed white line (A,B,B',C,C') indicates the ventricular surface. CTX, cortex; GE, ganglionic eminence. Scale bar: 100 µm.

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