The alternatively spliced
daf-2b transcript in Caenorhabditis elegans encodes a truncated isoform of the nematode insulin receptor that retains the extracellular ligand binding domain but lacks the intracellular signaling domain and is therefore unable to transduce a signal. To identify factors that influence expression of
daf-2b, we performed a targeted RNA interference screen of rsp genes which encode splicing factors from the serine/arginine protein family. Loss of
rsp-2 significantly increased the expression of a fluorescent
daf-2b splicing reporter, as well as increasing expression of endogenous
daf-2b transcripts. Correspondingly,
rsp-2 mutants exhibited similar phenotypes to those previously observed with DAF-2B overexpression, namely suppression of pheromone-induced dauer formation, enhancement of dauer entry in insulin signaling mutants, inhibition of dauer recovery and increased lifespan. However, the epistatic relationship between
rsp-2 and
daf-2b varied according to the experimental context. Increased dauer entry and delayed dauer exit of
rsp-2 mutants in an insulin signaling mutant background was partially dependent on
daf-2b. Conversely, suppression of pheromone-induced dauer formation and increased lifespan in
rsp-2 mutants were independent of
daf-2b. These data demonstrate that C. elegans RSP-2, an ortholog of human splicing factor protein SRSF5/SRp40, is involved in regulating the expression of the truncated DAF-2B isoform. However, we also find that RSP-2 can influence dauer formation and lifespan independently of DAF-2B.