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Fig. 4 The fin defects of unm_t30922t30922 mutants can be phenocopied by loss and rescued by gain of Wnt10a function. (A, B) Morpholino knockdown of wnt10a (A) or inhibition of canonical Wnt signaling via temporally controlled transgenic expression of dkk1 from 24 or 48 hpf onwards (B) both phenocopy the median fin fold collapse observed in the unm_t30922t30922 mutant embryos at 3 dpf. (C) Transgene-encoded wild-type wnt10a can fully rescue MFF collapse of unm_t30922t30922 mutants at 3 dpf when expressed from 24 hpf onwards, but can only rescue partially when expressed from 48 hpf onwards. (D) At 14 dpf (SL 5 mm), unm_t30922t30922 mutants lack most of their MFFs with the exception of the caudal fin. Similar to the effects at 3 dpf, mutants with transgenic expression of wild-type wnt10a from 24 to 144 hpf have regular MFFs, while mutants with transgenic expression of wild-type wnt10a from 48 to 144 hpf lack parts of their MFFs. (E) Despite the complete or partial MFF rescue at 3 and 14 dpf, mutants with transgene-driven wild-type wnt10a expression from 24 or 48 to 144 hpf have failed to develop complete adult fins at 31 dpf (SL 9 mm), resembling unm_t30922t30922 mutants without forced wild-type wnt10a expression. Arrowheads indicate collapsed fin folds and remnants of adult fins. MFF, median fin fold; SL, standard length.