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. 2019 Jan;14(1):59–61. doi: 10.4103/1673-5374.243703

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Copyright: © Neural Regeneration Research

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Sonic Hedgehog (Shh)-dependent morphological, cellular and molecular alterations in the dentate gyrus (DG) of Ptch1^+/– mice.

Schematic model in which Shh pathway activation positively feeds into the activities of the Notch signaling pathway resulting in upregulation of TLX, a direct target of Notch1/recombining binding protein suppressor of hairless (RBPJ), positively regulated by Sex determining region Y (SRY) box 2 (Sox2) and overexpressed in the DG of Ptch1^+/– mice. TLX is a critical transcription factors for balancing neural stem cells (NSCs) maintenance with neuronal differentiation and its upregulation is likely to promote neurogenic division and repress terminal differentiation, leading to tumor antigen presenting (TAP) cells accumulation and depletion of newborn neurons and astrocytes. The outcomes of this dysregulation are cellular and molecular defects in the hippocampus of Ptch1^+/– mice associated with DG elongation, and alterations in mouse behaviour. Significantly up- and down-regulated genes are indicated in red and blue, respectively. Activation (arrow lines); inhibition (cut lines). Modified from Antonelli et al. (2018). GFAP: Glial fibrillary acidic protein; RGL: radial glia-like cells; DCX: doublecortin; Ptch1: Patched1.