Fig. 2 Tp53 knockdown rescues wnt1 MO phenotypes. In situ hybridization was performed to detect deltaA (A, H, O), deltaB (B, I, P), neurog1 (C, J, Q), ascl1a (D, K, R), ascl1b (E, L, S), rfng (F, M, T), and sema3gb (G, N, U) in embryos injected with control (A–G), wnt1 (H–N), and wnt1 + tp53 (O–U) morpholinos. Loss of expression of deltaA, deltaB, neurog1, ascl1a, and ascl1b in the hindbrain of wnt1 morphant embryos (compare A–E with H–L) is rescued when Tp53 is knocked down (compare H–L with O–S). Expanded expression of boundary markers rfng and sema3gb in wnt1 morphant embryos (compare F and G with M and N) is also rescued by Tp53 knockdown (compare M and N with T and U).
Reprinted from Developmental Biology, 350(2), Gerety, S.S., and Wilkinson, D.G., Morpholino artifacts provide pitfalls and reveal a novel role for pro-apoptotic genes in hindbrain boundary development, 279-289, Copyright (2011) with permission from Elsevier. Full text @ Dev. Biol.