Figure 4.
hbl-1(RNAi) suppresses puf-9(ok1136) adult alae phenotypes while puf-9(RNAi) is unable to suppress a strong loss-of-function hbl-1 allele. (A) hbl-1(RNAi) suppresses the puf-9(ok1136) adult alae phenotypes. The number of puf-9(ok1136) animals displaying incomplete alae was decreased on hbl-1(RNAi) (n=55) compared to puf-9(ok1136) mutants alone (n=59). (B, left data sets) puf-9 is unable to suppress the hbl-1(ve18) precocious alae phenotype. hbl-1(ve18) mutants on mock RNAi (n=76) show a complete penetrance of precocious alae in the early L4 stage and nearly all hbl-1(ve18); puf-9(RNAi) animals (n=96) continued to display this precocious alae defect. (B, middle and right data sets) The precocious alae phenotypes of a weak hbl-1 allele and hbl-1(RNAi) are partially suppressed by removal of puf-9. hbl-1(mg285) animals exposed to puf-9(RNAi) (n=133) show a reduction in the number of animals displaying precocious alae at the early L4 stage, compared with mock RNAi (n=77). Similarly, puf-9(ok1136) mutants on hbl-1(RNAi) (n=75) suppressed the precocious alae seen with hbl-1(RNAi) exposure in a wild type background (n=69). puf-9(ok1136) mutant animals did not show any precocious alae on their own when fed mock RNAi (n=43). Error bars indicate standard deviations.