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Fig. 2. Gli1-mediated Cre recombination in proliferation EGL, ML, and GCL. (A) Schematic experimental design for the tamoxifen injection time points used in Gli1CreERT2/+:: R26RYFP/+ mice. Pups were orally injected TAM at P4-7 and sacrificed at P9 to analyze the YFP-expressing cells. (B) YFP labeled cells following tamoxifen injection are dominantly distributed in EGL, ML, and GCL in cerebellar cortex of the P9 Gli1CreERT2/+:: R26RYFP/+ pups. The lobules of vermis are identified by Roman numerals (II-X). Boxed region denotes enlarged area in C and D. (C, D) Triple staining for YFP, NeuN (a marker for GCs), PCP2 (a marker of PCs) and/or GFAP (a marker of BGs) of sagittal cerebellum of Gli1CreERT2/+:: R26RYFP/+ showed that YFP signal was colocalized with NeuN+ proliferating GCPs in EGL (C), differentiated GCNs in ML (C’~C”), GFAP+ BGs in ML/PCL (D~D”), but not in PCP2+ PCs (D and D”). Boxed region in C and D denotes enlarged area in C’, C”, D’ and D”. In D”. Asterisks indicated soma of PCs. P, postnatal day; TAM, tamoxifen; IHC, Immunohistochemistry; EGL, external granule cell layer; ML, Molecular layer; PCL, Purkinje cell layer; GCL, Granule cell layer. Scale bars=500 μm in B, 50 μm in C and D, 20 μm in C’~D”.
Exp Neurobiol 2021;30:203~212
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