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Fig. 5

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ZDB-IMAGE-210510-26
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Figures for Zhang et al., 2020
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Fig. 5 Cre and pknox binding sites in close vicinity to SBM1 and − 2 are necessary for the full activity of id1‐CRM2. A‐E, Immunohistochemistry with a GFP antibody on telencephalic cross sections of the id1‐CRM2 transgenic lines containing a mutation in the foxA2 (B), cre (C), pknox (D), and egr1 (E) binding sites, respectively. Mutation in cre (C) and pknox (D) binding sites leads to a reduction of GFP+ cells in the ventricular zone. F, G, J, Expression of the id1‐CRM2‐mut‐cre construct is inducible by brain injury (white asterisk, left injured hemisphere). G‐J, Magnification boxed area in F. K, L, O, Expression of the id1‐CRM2‐mut‐pknox construct is induced upon brain injury (white asterisk, left injured hemisphere). L‐O, Magnification of boxed area in K. Anterioposterior positions of transverse sections are indicated in the upper right‐hand corner of each image. P, Q, Percentage of GFP+/S100β+ RGCs over the total number of S100+ RGCs for id1‐CRM2 mutant constructs under homeostatic condition (P) and at 5 days postinjury, comparing the injured hemisphere (green columns) and the contralateral uninjured hemisphere (white columns; Q) at the dorsomedial to the dorsolateral region of the telencephalon. Scale bar = 200 μm (A‐F and K); 25 μm (G‐J and L‐O)

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