Abstract
In C. elegans embryogenesis, the MS blastomere produces predominantly mesodermal cell types, while its sister E generates only endodermal tissue. We show that a maternal gene, pop-1, is essential for the specification of MS fate and that a mutation in pop-1 results in MS adopting an E fate. Previous studies have shown that the maternal gene skn-1 is required for both MS and E development and that skn-1 encodes a transcription factor. We show here that the pop-1 gene encodes a protein with an HMG box similar to the HMG boxes in the vertebrate lymphoid-specific transcriptional regulators TCF-1 and LEF-1. We propose that POP-1 and SKN-1 function together in the early embryo to allow MS-specific differentiation.
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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Base Sequence
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Blastomeres / physiology
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Caenorhabditis / embryology*
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Caenorhabditis elegans Proteins*
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Cell Nucleus / genetics
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DNA-Binding Proteins / genetics*
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Embryo, Nonmammalian / physiology
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Gene Expression Regulation, Developmental / genetics
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Genes, Helminth / genetics
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Genes, Homeobox*
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High Mobility Group Proteins / genetics*
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Homeodomain Proteins / genetics*
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Mesoderm / physiology
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Molecular Sequence Data
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Mutation / genetics
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Pharynx / embryology
Substances
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Caenorhabditis elegans Proteins
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DNA-Binding Proteins
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High Mobility Group Proteins
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Homeodomain Proteins
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pop-1 protein, C elegans