Fig. 6 Atoh7 Loss of Function and Notch Activation Can Rescue Late Cell Fates in moks309
(A–D) Compared to wild-type (A), mok mutants (B) have an excess of RGCs and few bipolar cells, labeled by PKCα immunoreactivity. lak (atoh7) mutants fail to generate RGCs and overproduce bipolar neurons (C). lak/mok double mutants have rescued bipolar cell production.
(E–H) Heat-shocked induction of an activated form of Notch receptor NICD at 32 hpf drives progenitors toward a Müller glia fate (GS positive) in both wild-type (G) and moks309 retinas (H). The presence of the transgenes (hsp:Gal4, UAS:NICD) has no effect on Müller glia differentiation in the absence of heat shock (E and F).
Scale bars, 100 μm.
Reprinted from Cell, 134(6), Del Bene, F., Wehman, A.M., Link, B.A., and Baier, H., Regulation of neurogenesis by interkinetic nuclear migration through an apical-basal notch gradient, 1055-1065, Copyright (2008) with permission from Elsevier. Full text @ Cell