Abstract
Gastrulation in C. elegans embryos involves formation of a blastocoel and the ingression of surface cells into the blastocoel. Mutations in the par-3 gene cause abnormal separations between embryonic cells, suggesting that the PAR-3 protein has a role in blastocoel formation. In normal development, PAR proteins localize to either the apical or basal surfaces of cells prior to blastocoel formation; we demonstrate that this localization is determined by cell contacts. Cells that ingress into the blastocoel undergo an apical flattening associated with an apical concentration of non-muscle myosin. We provide evidence that ingression times are determined by genes that control cell fate, though interactions with neighboring cells can prevent ingression.
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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Animals
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Caenorhabditis elegans / cytology
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Caenorhabditis elegans / embryology*
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Caenorhabditis elegans / growth & development
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Caenorhabditis elegans / physiology
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Caenorhabditis elegans Proteins*
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Cell Lineage
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Cell Polarity*
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Embryo, Nonmammalian / physiology*
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Embryo, Nonmammalian / ultrastructure
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Gastrula / physiology*
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Genes, Reporter
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Helminth Proteins / genetics
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Helminth Proteins / metabolism*
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Morphogenesis
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Protein Serine-Threonine Kinases
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Recombinant Fusion Proteins / genetics
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Recombinant Fusion Proteins / metabolism
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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Recombinant Fusion Proteins
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PAR-3 protein, C elegans
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Protein Serine-Threonine Kinases