Fig. 4

The dorsal shift of the pallial-subpallial boundary upon loss of PAX6 is restored when LHX2 is also removed. a-d Tamoxifen was administered at E8.5 to Control (a), CreER;Lhx2 ^lox/lox (b), CreER;Pax6 ^lox/lox (c), and CreER;Lhx2 ^lox/lox ;Pax6 ^lox/lox(d) animals, and the embryos were harvested at E12.5. Coronal sections were examined for the expression of pallial marker Neurog2, subpallial markers Gsx2, and antihem marker Dbx1. The pallial-subpallial boundary (open arrowheads, a-d) appears to be normally positioned upon loss of LHX2 alone (b), but shifts dorsally upon loss of PAX6 alone, and Dbx1 expression is lost (c). Upon combined loss of both LHX2 and PAX6, the pallial-subpallial boundary appears to be restored to its normal position, together with Dbx1 expression. Loss of LHX2 results in lowered expression of Gsx2 in the subpallium compared with control brains (a, b, d). e Cartoons schematizing the results in a-d. f A model of the interactions between Lhx2, Gsx2, and Pax6 upon the hem and the antihem. Solid blue lines indicate regulatory functions identified in this study: LHX2 maintains Gsx2 expression levels in the ventral telencephalon, and PAX6 suppresses hem fate in the dorsolateral telencephalon. The dotted blue line indicates that regulation of Dbx1 by PAX6 is likely to be indirect. Scale bar is 200 μm