Abstract
Mutations in the C. elegans gene egl-27 cause defects in cell polarity and cell migration: the polarity of the asymmetric T cell division is disrupted and the descendants of the migratory QL neuroblast migrate incorrectly because they fail to express the Hox gene mab-5. Both of these processes are known to be controlled by Wnt pathways. Mosaic analysis indicates that egl-27 function is required in the T cell for proper cell polarity. We cloned egl-27 and discovered that a domain of the predicted EGL-27 protein has similarity to Mta1, a mammalian factor overexpressed in metastatic cells. Overlaps in the phenotypes of egl-27 and Wnt pathway mutants suggest that the EGL-27 protein interacts with Wnt signaling pathways in C. elegans.
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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Animals, Genetically Modified
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Base Sequence
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Caenorhabditis elegans / embryology
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Caenorhabditis elegans Proteins*
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Cell Movement*
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Cell Polarity*
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Cloning, Molecular
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DNA, Complementary
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DNA-Binding Proteins*
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Gene Expression Regulation, Developmental
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Helminth Proteins / genetics*
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Helminth Proteins / physiology
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Histone Deacetylases*
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Humans
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Molecular Sequence Data
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Proteins / genetics*
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RNA, Messenger
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Rats
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Repressor Proteins*
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Sequence Homology, Amino Acid
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T-Lymphocytes
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Trans-Activators
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Transcription Factors*
Substances
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Caenorhabditis elegans Proteins
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DNA, Complementary
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DNA-Binding Proteins
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EGL-27 protein, C elegans
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Helminth Proteins
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MTA1 protein, human
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Proteins
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RNA, Messenger
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Repressor Proteins
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Trans-Activators
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Transcription Factors
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Histone Deacetylases