Gene expression in the pharynx is regulated by organ-specific signals, which in the
myo-2 enhancer target a short DNA sequence termed the C sub-element. To begin to understand these signals, we performed a one hybrid screen in yeast to identify C. elegans cDNAs encoding factors that bind the C sub-element (see abstract by Thatcher and Okkema). One of the clones identified in this screen is from the
daf-3 gene, which is required for dauer formation. To understand the role of
daf-3 in controlling pharyngeal gene expression, C sub-element activity was examined in
daf-3 mutants, as well as in other daf mutants. Surprisingly, these results indicate
daf-3 is a negative regulator of C sub-element activity. Although expression of a C sub-element driven reporter in a
daf-3 null mutant was similar to wild type, expression was reduced by a mutation in
daf-4, a negative regulator of
daf-3. Furthermore, a
daf-3 mutation suppresses the
daf-4 phenotype in
daf-4;
daf-3 double mutants, demonstrating that the
daf-4 repression requires wild type
daf-3.
daf-3 encodes a mothers against dpp (SMAD) homolog (see abstract by Patterson and Ruvkun). SMAD proteins are downstream components of TGFb like signaling pathways, but are not known to bind DNA directly. Attempts to demonstrate binding of DAF-3 to the C sub-element in vitro have not yet been successful, so it remains unclear how
daf-3 controls C sub-element activity. These results indicate the C sub-element is targeted by the TGFb like signaling pathway controlling dauer formation, and suggest that intercellular signaling is involved in regulation of pharyngeal gene expression.