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Fig. 3
Degeneration of the retina of dn-fgfr1 transgenic animals over time.
A, E) Control (ctrl) and Tg(hsp70l:dnfgfr1-EGFP) (dn-fgfr1) siblings without heat shock (HS) treatment: in both cases no morphological changes were detected B–D) In control siblings, the architecture of the retina and the thickness of the ONL (indicated by the error bar) remains unaffected F–H) In contrast, in transgenic animals a decrease in organization and in the width of the ONL (indicated by decreasing size of error bars) is observed. D2, H2) Insets show the normal structure of control retina and the changes in the retinas of dn-fgfr1 animals. In dn-fgfr1 transgenics, vacuoles appear in the RPE (white arrowhead), and the thickness of the RPE increases. The POS and ONL decrease in thickness. For orientation purposes, the black arrowheads indicate the border of horizontal cells. I) An activated Caspase-3 positive cell in the ONL (white arrowhead) after heat shock treatment on three consecutive days. J) Activated Caspase-3 positive cells in the INL and ONL (arrowheads) after five days of Fgf signaling inhibition. G) Quantifications of activated Caspase-3 positive cells per section over time. In wild-type and transgenic fish without any heat shock, dying cells are not detectable (p = 2,28). After three days of heat shock treatment dying cells are detected in the transgenic fish only in the ONL (grey column) (p = 2,44E-08). After five (p = 1,04E-41) and seven days, an increased number of activated Caspase-3 positive cells are in both the ONL (grey column) and INL (black column) (p = 6,42E-26). Shown are the mean numbers of Casp3+ cells/section. Error bars indicate the standard error of the mean (SEM). p-values: *d0.05, **d0.01, ***d0.001. ctrl, control; HS, heat shock; dn-fgfr1, Tg(hsp70l:dnfgfr1-EGFP). Scale bars = 20 μm.