Abstract
After the first division of the C. elegans embryo, the posterior blastomere can produce numerous muscles while the anterior blastomere cannot. We show here that maternal-effect lethal mutations in the gene mex-3 cause descendants of the anterior blastomere to produce muscles by a pattern of development similar to that of a descendant of the wild-type posterior blastomere. mex-3 encodes a probable RNA-binding protein that is distributed unequally in early embryos and that is a component of germline-specific granules called P granules. We propose that MEX-3 contributes to anterior-posterior asymmetry by regulating one or more mRNAs involved in specifying the fate of the posterior blastomere.
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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Alleles
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Animals
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Base Sequence
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Blastomeres / cytology*
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Caenorhabditis elegans / embryology*
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Caenorhabditis elegans Proteins*
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Cytoplasm / metabolism
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Cytoplasmic Granules / metabolism
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Gene Expression Regulation, Developmental
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Genes, Helminth
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Genes, Lethal
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Helminth Proteins / physiology*
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Humans
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In Situ Hybridization
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Molecular Sequence Data
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Morphogenesis
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Muscles / embryology
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RNA, Messenger / metabolism
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RNA-Binding Proteins / genetics*
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Sequence Alignment
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Sequence Homology, Amino Acid
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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MEX-3 protein, C elegans
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RNA, Messenger
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RNA-Binding Proteins