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doi:10.1534/genetics.105.052621
A more recent version of this article appeared on December 1, 2006.
REGULAR RESEARCH PAPERS |
Reduced dosage of pos-1 suppresses Mex mutants and reveals complex interactions among CCCH zinc-finger proteins during Caenorhabditis elegans embryogenesis
Jennifer R. Tenlen 1, Jennifer A. Schisa 2, Scott J. Diede 3 and Barbara D. Page 1*
1 Fred Hutchinson Cancer Research Center
2 Central Michigan University
3 Children's Hospital and Regional Medical Center
* To whom correspondence should be addressed. E-mail: bdpage{at}gmail.com.
Submitted on January 18, 2006
Revised on March 29, 2006
Accepted on 11 September 2006
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 proteins' functions reveal complex interactions among the CCCH finger proteins and suggest that their complementary expression patterns might be refined by antagonistic interactions among them.
Key Words: CCCH zinc finger, MEX-5, POS-1, cell fate specification
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