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Originally published as Genetics Published Articles Ahead of Print on October 8, 2006.

Genetics, Vol. 174, 1933-1945, December 2006, Copyright © 2006
doi:10.1534/genetics.105.052621

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Reduced Dosage of pos-1 Suppresses Mex Mutants and Reveals Complex Interactions Among CCCH Zinc-Finger Proteins During Caenorhabditis elegans Embryogenesis

Jennifer R. Tenlen*,{dagger},1, Jennifer A. Schisa{ddagger},1, Scott J. Diede§ and Barbara D. Page*,**,2

* Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, ** Howard Hughes Medical Institute, Seattle, Washington 98109, {dagger} Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, § Children's Hospital and Regional Medical Center, Department of Hematology and Oncology, Seattle, Washington 98105 and {ddagger} Department of Biology, Central Michigan University, Mount Pleasant, Michigan 48859

2 Corresponding author: Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, Mailstop c3-168, Seattle, WA 98109.
E-mail: bdpage{at}gmail.com

Cell fate specification in the early C. elegans embryo requires the activity of a family of proteins with CCCH zinc-finger motifs. Two members of the family, MEX-5 and MEX-6, are enriched in the anterior of the early embryo where they inhibit the accumulation of posterior proteins. Embryos from mex-5 single-mutant mothers are inviable due to the misexpression of SKN-1, a transcription factor that can specify mesoderm and endoderm. The aberrant expression of SKN-1 causes a loss of hypodermal and neuronal tissue and an excess of pharyngeal muscle, a Mex phenotype (muscle excess). POS-1, a third protein with CCCH motifs, is concentrated in the posterior of the embryo where it restricts the expression of at least one protein to the anterior. We discovered that reducing the dosage of pos-1(+) can suppress the Mex phenotype of mex-5(–) embryos and that POS-1 binds the 3'-UTR of mex-6. We propose that the suppression of the Mex phenotype by reducing pos-1(+) is due to decreased repression of mex-6 translation. Our detailed analyses of these protein functions reveal complex interactions among the CCCH finger proteins and suggest that their complementary expression patterns might be refined by antagonistic interactions among them.




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