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Fig. 7 | Neural Development

Fig. 7

From: Genetic deletion of genes in the cerebellar rhombic lip lineage can stimulate compensation through adaptive reprogramming of ventricular zone-derived progenitors

Fig. 7

Inactivation of Gli2 in both Nestin- and Atoh1-expressing cells inhibits the recovery of the CB compared to in mice lacking Gli2 only in the EGL. a, c, e and g H&E of sagittal sections of the cerebellar vermis of P12 Gli2flox/flox (Control, a), Nes-FlpoER/+; R26MASTR/+; Gli2flox/flox (Nes-Gli2 CKO, c), Atoh1-Cre/+; Gli2flox/flox (Atoh1-Gli2 CKO, e), and Atoh1-Cre/+; Nes-FlpoER/+; R26MASTR/+; Gli2flox/flox (Atoh1-Nes-Gli2 CKO, g) mice injected with Tm at P0. Note that inactivation of Gli2 only in Nestin-expressing cells has no major effect of CB development at P12. However, inactivation of Gli2 in Nestin-expressing cells inhibits the compensation mechanism when Gli2 is removed in GCPs (g compared to e). b, d, f and h High magnifications (as shown by yellow squares in (a, c, e and g) of anterior vermis of P12 Gli2flox/flox (b), Nes-FlpoER/+; R26MASTR/+; Gli2flox/flox (Nes-Gli2 CKO, d), Atoh1-Cre/+; Gli2flox/flox (Atoh1-Gli2 CKO, f), and Atoh1-Cre/+; Nes-FlpoER/+; R26MASTR/+; Gli2flox/flox (Atoh1-Nes-Gli2 CKO, h) cerebella stained with the indicated proteins and dapi. White arrowhead and white asterisk indicate the loss of EGL and IGL respectively in Atoh1-Nes-Gli2 CKO. Scale bars represent 1 mm (a, c, e and g) and 100 μm (b, d, f and h)

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