Abstract
In vertebrates, wnt8 has been implicated in the early patterning of the mesoderm. To determine directly the embryonic requirements for wnt8, we generated a chromosomal deficiency in zebrafish that removes the bicistronic wnt8 locus. We report that homozygous mutants exhibit pronounced defects in dorso-ventral mesoderm patterning and in the antero-posterior neural pattern. Despite differences in their signaling activities, either coding region of the bicistronic RNA can rescue the deficiency phenotype. Specific interference of wnt8 translation by morpholino antisense oligomers phenocopies the deficiency, and interference with wnt8 translation in ntl and spt mutants produces embryos lacking trunk and tail. These data demonstrate that the zebrafish wnt8 locus is required during gastrulation to pattern both the mesoderm and the neural ectoderm properly.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Body Patterning / physiology*
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Cytoskeletal Proteins
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Ectoderm / physiology
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Fetal Proteins
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Gene Expression Regulation, Developmental
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Head / embryology
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Mesoderm / physiology
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Molecular Sequence Data
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Mutagenesis / physiology
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Oligonucleotides, Antisense
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Open Reading Frames
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Phenotype
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Proteins / genetics*
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RNA, Messenger / genetics
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T-Box Domain Proteins / genetics
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Tail / embryology
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Transcription, Genetic / physiology*
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Wnt Proteins
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Zebrafish / embryology*
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Zebrafish Proteins / genetics*
Substances
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Cytoskeletal Proteins
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Fetal Proteins
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Oligonucleotides, Antisense
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Proteins
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RNA, Messenger
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T-Box Domain Proteins
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Wnt Proteins
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Zebrafish Proteins
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tbx16 protein, zebrafish
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wnt8a protein, zebrafish
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Brachyury protein
Associated data
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GENBANK/AY032748
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GENBANK/AY032749