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. Author manuscript; available in PMC: 2010 Oct 1.
Published in final edited form as: Genesis. 2009 Oct;47(10):667–673. doi: 10.1002/dvg.20546

Figure 4. Misexpression of Gbx2 in the ventral telencephalon does not result in gross defects in neurons derived from the Nkx2.1 lineage.

Figure 4

(A) X-gal histochemistry of coronal sections of Nkx2.1-Cre; R26R embryos at E12.5. Note that Nkx2.1-expressing cells and their descendants contribute widely to the ventral telencephalon and the cortex (arrowheads). (B–C) In situ hybridization of Gbx2 on coronal sections of control (B) and Nkx2.1-Cre; Gbx2-GOF double transgenic (C) embryos at E12.5. Dashed circle marks the endogenous Gbx2 expression in MGE mantle zone; asterisk indicates ectopic expression of Gbx2 in MGE ventricular zone. (D–I) X-gal histochemical analysis on coronal sections of adult Gbx2-GOF hemizygous mice with and without the Nkx2.1-Cre transgene as indicated. Boxed areas in D and E corresponding to the globus pallidus and hypothalamus are magnified in F–I.