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The MEP-1 zinc-finger protein acts with MOG DEAH box proteins to control gene expression via the fem-3 3′ untranslated region in Caenorhabditis elegans

Published online by Cambridge University Press:  20 August 2002

MARCO BELFIORE
Affiliation:
Department of Zoology, University of Fribourg, Pérolles, CH-1700 Switzerland
LAURA D. MATHIES
Affiliation:
Department of Biochemistry, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA Howard Hughes Medical Institute, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA
PAOLO PUGNALE
Affiliation:
Department of Zoology, University of Fribourg, Pérolles, CH-1700 Switzerland
GARY MOULDER
Affiliation:
Program in Molecular Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
ROBERT BARSTEAD
Affiliation:
Program in Molecular Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
JUDITH KIMBLE
Affiliation:
Department of Biochemistry, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA Howard Hughes Medical Institute, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA
ALESSANDRO PUOTI
Affiliation:
Department of Zoology, University of Fribourg, Pérolles, CH-1700 Switzerland
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Abstract

Cell fates in the Caenorhabditis elegans germline are regulated, at least in part, at the posttranscriptional level. For example, the switch from spermatogenesis to oogenesis in the hermaphrodite relies on posttranscriptional repression of the fem-3 mRNA via its 3′ untranslated region (UTR). Previous studies identified three DEAH box proteins, MOG-1, MOG-4, and MOG-5, that are critical for the fem-3 3′ UTR control. Here we describe MEP-1, a zinc-finger protein that binds specifically to each of these three MOG proteins and that is required for repression by the fem-3 3′ UTR in vivo. To investigate its in vivo function, we generated a mep-1 deletion mutant. The mep-1 null phenotype suggests a broad role for MEP-1 in C. elegans development, as it is associated with early larval arrest. In addition, mep-1 mutants can be defective in gonadogenesis and oocyte production when derived from a heterozygous mother. We suggest that MEP-1 acts together with the MOG proteins to repress fem-3 mRNA and that it also functions in other pathways to control development more broadly.

Type
Research Article
Copyright
© 2002 RNA Society

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