1. EGL-27 is similar to a metastasis-associated factor and controls cell polarity and cell migration in C. elegans.
- Author
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Herman MA, Ch'ng Q, Hettenbach SM, Ratliff TM, Kenyon C, and Herman RK
- Subjects
- Amino Acid Sequence, Animals, Animals, Genetically Modified, Base Sequence, Caenorhabditis elegans embryology, Cloning, Molecular, DNA, Complementary, Gene Expression Regulation, Developmental, Helminth Proteins physiology, Humans, Molecular Sequence Data, RNA, Messenger, Rats, Sequence Homology, Amino Acid, T-Lymphocytes, Trans-Activators, Caenorhabditis elegans Proteins, Cell Movement, Cell Polarity, DNA-Binding Proteins, Helminth Proteins genetics, Histone Deacetylases, Proteins genetics, Repressor Proteins, Transcription Factors
- 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.
- Published
- 1999
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