Cellular organization, her phenotypes and her genetic interactions in the TPZ. (A-C) Cellular organization in the TPZ. (A) Horizontal plane dorsal view, plane indicated in B, which shows parasagittal section indicated in A. (C) Marker expression. Magenta cells, Sox2high nuclei of the telencephalic ventricular wall, her expression not determined. White cells not analyzed for markers. Gray cells, differentiating early and mature neurons, some of which express neurod family members. (D-G) Schematic of TPZ Sox2 expression in WT and mutants as indicated. Sox2high (NSCs) in dark magenta, Sox2low (NPCs) in light magenta. ‘V’ magenta, Sox2high -and her6 high-expressing cells only present in lateral ventricle wall. Black lines, ventricular surface. Dotted line in G, impairment of ventricle wall integrity. (H) Postulated her gene network interactions. Boxes show analyzed genes and gene expression. Lines indicate how mutations or overexpression influence expression of other genes, interactions may not be direct. Black lines, functional compensation (dot indicates directionality). Dashed black line, partial compensation of her6 and her9 loss. Green inhibition signs, autoregulation of her6 and her9, and postulated negative autoregulation in the her4;her12 and her2;her15 clusters. Blue influence signs, changed Sox2 and neurog1 expression in her6,her9 double mutants. Blue dashed influence sign, loss of Notch-dependent her activity in Df(her4;12),Df(her2;15) only affects Sox2 expression in herUDMs. Red inhibition signs, downregulation of genes upon overexpression of her6 or her4. Dashed red inhibition sign indicates mild downregulation of ascl1b by her4 overexpression. A-P, anterior-posterior; cth, caudal thalamus; D-V, dorsal-ventral; ptec, pretectum; pth, prethalamus (ventral thalamus), rth, rostral thalamus; tec, tectum opticum; tel, telencephalon; th, thalamus; ve, ventricle.