Fig. 8

Depletion of mllt10/af10 and dot1l rescues intestinal defects in apc^mcr/mcr zebrafish, mimicking tcf7l2 depletion.
Depletion of mllt10/af10 and dot1l rescues expression of i-fabp in apc^mcr/mcr mutant embryos, placing these genes downstream of Apc as Wnt target gene activators (A–N). Representative whole mount in situ hybridizations for i-fabp in wild type and apc^mcr/mcr mutant embryos at 80 hpf injected with (A,B) buffer alone,(C,D) MO against tcf7l2, (E–H) two independent mllt10/af10 MOs, (I–L) two independent dot1l MO, and (M,N) control MO. Depletion of mllt10/af10 and dot1l rescues mis-expression of cyp26a1 in apc^mcr/mcr mutant embryos (O–AB). Representative whole mount in situ hybridizations for cyp26a1 in wild type and apc^mcr/mcr mutant embryos at 80 hpf injected with (O,P) buffer alone, (Q,R) MO against tcf7l2, (S–V) two independent mllt10/af10 MOs, (W–Z) two independent dot1l MO, and (AA,AB) control MO. All MOs have been coinjected with an MO against p53. All images were captured using the same exposure and represent at least three independent experiments. In parentheses number of embryos showing described phenotype per number of total embryos analyzed.