Fig. 2. Mash1 mutants have a defect in the production of early-born (N1) neurons and their VZ cells precociously acquire SVZ-like properties. Fluorescence and darkfield microscopic images of coronal hemi-sections of control (left side) and Mash1 mutant (right side) telencephalons at E10.5 (A-C'), E11.5 (D-I', E15.5 (J-K') and E18.5 (L,L'). The sections were stained with antibodies directed to the antigens, or ³⁵S-labeled probe, listed above each panel. Yellow cells are double-labeled. While Mash1 mutants produce few MAP2+ cells at E10.5 (N1 cells; A-B'), their progenitor zone appears to mature precociously based on the increased number of cells that express DLX2 (C,C',F,F'). These DLX2 cells are mitotically active precursors, based on co-expression with PCNA (arrow in F'). At E11.5, the mutant LGE produces many GABA+ cells (arrow E''), but most of these do not express MAP2. We suggest that a substantial number of the MAP2-expressing cells adjacent to the LGE in D' (arrowhead) are not produced by the LGE, but rather correspond to ventral pallial cells (see arrowhead in G' for pattern of Lhx2 expression, which marks the mantle of the ventral pallium, VP). Note the paucity of MAP2 expression in the MGE mantle (D') while GABA expression on the same section is abundant (E'). Mash1 also has later functions in subcortical development. At E15.5 and E18.5 there is ectopic expression of GABA in the progenitor zone of the LGE. Arrowhead in K' indicates ectopic GABA expression; arrows in L,L' indicate LGE proliferative zones. ctx, cortex; LV, lateral ventricle; MGE, medial ganglionic eminence; st, striatum. Scale bars: 100 µm.

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