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Fig. 7. piy-mediated apoptosis depends on the ATM-Chk2-p53 pathway.
(A) Quantitative PCR analysis of p53 mRNA in wild-type and
piy mutant zebrafish embryos. There is no difference in the
amplification of a control gene, ef1
(lower panel), from
wild-type and the piy mutant cDNA pools. By contrast, the
p53 gene is amplified from the piy mutant cDNA pool by a
smaller number of PCR cycles than from the wild-type cDNA pool (upper panel),
suggesting that p53 mRNA is more abundant in the piy mutant
embryos than in wild-type embryos. (B,C) Plastic sections of
piy mutant retinas injected without (B) and with (C) MO-Chk2.
(D,E) Plastic sections of piy mutant retinas injected
without (D) and with (E) MO-p53. (F-H) Treatment of the piy
mutant embryos with DMSO (F), KU55933 (G) or CGK733 (H). (I-K) Labeling
of wild-type sibling (I), piy mutant (J) and MO-p53-injected
piy mutant (K) retinas with the zn5 antibody, which labels RGCs
(red). All nuclei are counterstained with Sytox Green (green). (L-N)
Labeling of wild-type sibling (L), piy mutant (M) and MO-p53 injected
piy mutant (N) retinas with the zpr1 antibody, which labels
double-cone type photoreceptors (red). (O-Q) Labeling of retinas of
piy mutant (O), OKR-restored MO-p53-injected piy mutant (P)
and OKR-restored MO-Chk2-injected piy mutant (Q) with anti-GABA
antibody (red). GABA expression is normal in RGCs and amacrine cells in both
MO-injected retinas.
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