High impact information on daf-3

• Null mutations in daf-3 suppress mutations in genes encoding this TGF-beta signal, its receptors, and associated Smad signal transduction proteins. daf-3 encodes a Smad protein that is most closely related to mammalian DPC4, and is expressed throughout development in many of the tissues that are remodeled during dauer development [1].
• We have studied the daf-5 gene, which, along with the daf-3 Smad gene, is antagonized by upstream receptors and receptor-regulated Smads [2].
• The Daf-c phenotype was suppressed by daf-7 cDNA expression or a daf-3 null mutation [3].
• To determine how daf-3 affects C subelement enhancer activity in vivo, we examined expression a gfp reporter controlled by a concatenated C subelement oligonucleotide in daf-3 mutants and other mutants affecting the TGFbeta-like signaling pathway controlling dauer formation [4].
• These results suggest daf-3 directly regulates pharyngeal gene expression during non-dauer development [4].

Biological context of daf-3

• Our results demonstrate that wild-type daf-3 can repress C subelement enhancer activity during larval development and, like its dauer-promoting activity, daf-3's repressor activity is negatively regulated by TGFbeta-like signaling [4].

Other interactions of daf-3

• Three complementation groups correspond to the previously described genes daf-3, daf-5, and daf-12 [5].

Analytical, diagnostic and therapeutic context of daf-3

• Mutation of any base in the sequence GTCTG interfered with binding in the gel mobility shift assay, demonstrating that this pentanucleotide is a core recognition sequence for DAF-3 binding. daf-3 is known to promote formation of dauer larvae and this activity is negatively regulated by TGFbeta-like signaling [4].

References