Abstract
beta-Catenin signaling determines the proximal-distal axis of the C. elegans gonad by promoting distal fate in asymmetrically dividing somatic gonad precursor cells (SGPs). Impaired function of the Wnt effector POP-1/TCF, its coactivator SYS-1/beta-catenin, and of upstream components including beta-catenin WRM-1 causes all SGP daughters to adopt the proximal fate. Consequently, no distal tip cells (DTCs) that would lead differentiation of gonad arms form in the affected hermaphrodites. Here, we show that deficiency of the nuclear receptor NHR-25 has the opposite effect: extra DTCs develop instead of proximal cells. NHR-25 knockdown restores DTC formation and fertility in pop-1 and sys-1 mutants, suggesting that a balance between NHR-25 and beta-catenin pathway activities is required to establish both proximal and distal fates. This balance relies on direct crossregulation between NHR-25 and the distinct beta-catenin proteins WRM-1 and SYS-1. The nuclear receptor-beta-catenin interaction may be an ancient mechanism of cell-fate decision.
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