Abstract
Mutations in the unc-39 gene of C. elegans lead to migration and differentiation defects in a subset of mesodermal and ectodermal cells, including muscles and neurons. Defects include mesodermal specification and differentiation as well a neuronal migration and axon pathfinding defects. Molecular analysis revealed that unc-39 corresponds to the previously named gene ceh-35 and that the UNC-39 protein belongs to the Six4/5 family of homeodomain transcription factors and is similar to human Six5, a protein implicated in the pathogenesis of type I myotonic dystrophy (DM1). We show that human Six5 and UNC-39 are functional homologs, suggesting that further characterization of the C. elegans unc-39 gene might provide insight into the etiology of DM1.
Publication types
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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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Base Sequence
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Caenorhabditis elegans / cytology*
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Caenorhabditis elegans / embryology
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Caenorhabditis elegans Proteins / genetics*
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Caenorhabditis elegans Proteins / metabolism*
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Cell Differentiation / physiology*
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Cell Movement / physiology
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Cheek / growth & development
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Ectoderm / physiology
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Embryo, Nonmammalian
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Embryonic Induction
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Female
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Gene Expression Regulation, Developmental
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Head / embryology
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Homeodomain Proteins / genetics*
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Homeodomain Proteins / metabolism*
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Humans
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Mesoderm / pathology
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Molecular Sequence Data
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Muscles / cytology
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Muscles / embryology
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Mutation
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Neurons / metabolism
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Neurons / pathology
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Pharynx / growth & development
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Sequence Homology, Amino Acid
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Vulva / cytology
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Vulva / embryology
Substances
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Caenorhabditis elegans Proteins
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Homeodomain Proteins
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SIX5 protein, human
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Unc-39 protein, C elegans