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Development, Vol 126, Issue 5 1055-1064, Copyright © 1999 by Company of Biologists
JOURNAL ARTICLES |
MA Herman, Q Ch'ng, SM Hettenbach, TM Ratliff, C Kenyon and RK Herman
Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
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.
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