Fig. 6. Dlx1/2 mutants show expanded Notch signaling domains and a block in differentiation of SVZ cells. Dark-field and fluorescence photomicroscopic images of coronal hemi-sections of control (left side) and Dlx1/2 mutant (right side) telencephalons at E15.5 (A-I') and E18.5 (J-L') studied using radioactive in situ hybridization (B-E',G-H',J,J') and immunofluorescence (A,A',I,I',K,K',L,L'). (G-H') The Dlx1/2 mutant SVZ shows elevated expression of VZ markers (COUP-TF1; Gsh2). These defects are correlated with increases in MASH1, Dll1 and Hes5 expression (A,A',D-E'), particularly in the SVZ. Note that while the Hes5 and Notch1 (E-F') expression domain expands, Hes1 and Notch3 (B-C') expression remains normal in the Dlx1/2 mutants. The persistence of progenitor molecular properties as late as E18.5 (not shown) is linked with persistent expression of a radial glial marker (RC2; L,L'). The defects in SVZ differentiation are correlated with reduced expression of striatal markers, such as dopamine receptor 2 (Drd2) (J,J'), while a general marker of neurogenesis (MAP2) appears normal in the mantle zone (I-K'). Note, however, that MAP2 expression extends much closer to the ventricle in the mutant at E18.5 (boxed areas in K,K'). ctx, cortex; ic, internal capsule; LV, lateral ventricle; spt, septum; st, striatum. Scale bars: 100 µm.

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