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First published online August 14, 2006
doi: 10.1242/10.1242/dev.02496

1 Zoologisches Institut, Universität Zürich, Winterthurerstrasse 190,
CH-8057, Zürich, Switzerland.
2 Molecular Life Science PhD Program, Molekular biologisches Institut,
Universität Zürich, Winterthurerstrasse 190, CH-8057, Zürich,
Switzerland.
Author for correspondence (e-mail:
ahajnal{at}zool.unizh.ch)
Accepted 15 June 2006
The C. elegans PUF and FBF proteins regulate various aspects of germline development by selectively binding to the 3' untranslated region of their target mRNAs and repressing translation. Here, we show that puf-8, fbf-1 and fbf-2 also act in the soma where they negatively regulate vulvaI development. Loss-of-function mutations in puf-8 cause ectopic vulval differentiation when combined with mutations in negative regulators of the EGFR/RAS/MAPK pathway and suppress the vulvaless phenotype caused by mutations that reduce EGFR/RAS/MAPK signalling. PUF-8 acts cell-autonomously in the vulval cells to limit their temporal competence to respond to the extrinsic patterning signals. fbf-1 and fbf-2, however, redundantly inhibit primary vulval cell fate specification in two distinct pathways acting in the soma and in the germline. The FBFs thereby ensure that the inductive signal selects only one vulval precursor cell for the primary cell fate. Thus, translational repressors regulate various aspects of vulval cell fate specification, and they may play a conserved role in modulating signal transduction during animal development.
Key words: Caenorhabditis elegans, Vulva, Pumilio, Translational control, Signal transduction
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