|
Fig. 5
Functional Investigation of Interaction Maps Reveals Fgf Signaling Controlling PC Proliferation
(A) tSNE plot (all cells on the left, progenitors on the right) for fgfr3, which is localized specifically to PCs.
(B) Predicted interaction map for fgfr3 and its ligands.
(C) Based on the interaction prediction, PC 2 and PC 5 are exposed to FGF signaling after amyloid treatment.
(D) Methodology for functional validation of the effects of FGF signaling on PC proliferation.
(E–H’) Immunohistochemical staining for PCNA in control (E–H) and FGF8-injected (E’–H’) adult zebrafish brains. Regional identities are indicated with the names denoted in (C). Panels E–H modified from Kizil and Brand, 2011.
(I) Quantification of regional proliferation response after FGF8-injection.
(J) Working model of the regulatory cascade of NSPC proliferation in the adult zebrafish brain by Aβ42-induced FGF signaling.
Three sections were quantified for every experimental group. Scale bars, 50 μm. Data are represented as mean ± SEM. The levels of significance are ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001.