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

Reduced Dosage of pos-1 Suppresses Mex Mutants and Reveals Complex Interactions Among CCCH... 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 ( m uscle ex cess). 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. Footnotes ↵ 1 These authors contributed equally to this work. Communicating editor: K. K emphues Received January 18, 2006. Accepted September 11, 2006. Copyright © 2006 by the Genetics Society of America http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genetics Genetics Society of America

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

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Publisher
Genetics Society of America
Copyright
Copyright © 2006 by the Genetics Society of America
ISSN
0016-6731
eISSN
1943-2631
D.O.I.
10.1534/genetics.105.052621
Publisher site
See Article on Publisher Site

Abstract

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 ( m uscle ex cess). 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. Footnotes ↵ 1 These authors contributed equally to this work. Communicating editor: K. K emphues Received January 18, 2006. Accepted September 11, 2006. Copyright © 2006 by the Genetics Society of America

Journal

GeneticsGenetics Society of America

Published: Dec 1, 2006

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