In a screen for suppressors of activated GOA-1 (Galpha(o)) under the control of the
hsp-16.2 heat-shock promoter, we identified three genetic loci that affected heat-shock-induced GOA-1 expression. The
cyl-1 mutants are essentially wild type in appearance, while
hsf-1 and
sup-45 mutants have egg-laying defects. The
hsf-1 mutation also causes a temperature-sensitive developmental arrest, and
hsf-1 mutants have decreased life span. Western analysis indicated that mutations in all three loci suppressed the activated GOA-1 transgene by decreasing its expression. Heat-shock-induced expression of
hsp-16.2 mRNA was reduced in
cyl-1 mutants and virtually eliminated in
hsf-1 and
sup-45 mutants, as compared to wild-type expression. The mutations could also suppress other transgenes under heat-shock control.
cyl-1 and
sup-45, but not
hsf-1, mutations suppressed a defect caused by a transgene not under heat-shock control, suggesting a role in general transcription or a post-transcriptional aspect of gene expression.
hsf-1 encodes the C. elegans homolog of the human heat-shock factor HSF1, and
cyl-1 encodes a cyclin most similar to cyclin L. We believe HSF-1 acts in heat-shock-inducible transcription and CYL-1 acts more generally in gene expression.