Fig. 9

Interaction between klf8, p53, and met regulates apoptosis in zebrafish embryos. (A–C) Decreased met expression in the tectum (arrowhead) and rhombomere 1 (asterisk) of klf8 morphants (B) relative to WT (A) can be rescued by co-injection of p53 MO^sp (C). (D) Percentage of embryos of the indicated backgrounds with decreased met expression relative to WT embryos. (E–G) Expression of p53 in the various brain regions at 24 hpf is detected in embryos co-injected with CM1 and CM2 (G), but not in WT (E) or in embryos injected with CM1mm (F). (H) Percentage of embryos of the indicated backgrounds with increased p53 expression relative to WT embryos. (I–L) Increased apoptosis in the cerebellar primordium at 24 hpf is observed in embryos co-injected with CM1 and CM2 (K) as compared with WT (I), or embryos injected with CM1mm (J). Co-injection of p53 MO^sp with CM1 and CM2 rescues the apoptosis defect (L). (M) Percentage of TUNEL-positive cells in the embryos of the indicated backgrounds relative to WT embryos. (N–R) Increased nuclear distribution of p53 in the cerebellar primordium of klf8 morphants (O) relative to WT (N) is reduced by co-injection with met mRNA (Q, R), but not with LacZ mRNA (P). (S–U) Increased p21 expression in the retinae and brain regions of klf8 morphants relative to WT (S) is rescued by co-injection with met mRNA (U), but not with LacZ mRNA (T). (V) Percentage of embryos of the indicated backgrounds with increased p21 expression relative to WT embryos. (W) A model describing how Klf8 regulates the maintenance of ptf1a-expressing neuronal progenitors by modulating expression of p53 and met. (A–C) lateral views; (E–G, I–L, N–U) dorsal views. Significance was determined using Student′s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. Error bars indicate standard errors. R1, rhombomere 1; te, tectum.