Figure 3. The mir-51 family members, mir-52 and mir-54/55/56 .

, function in multiple miRNA-dependent developmental pathways. (A, B) mir-52 suppresses ASEL specification defects of lsy-6(rf)/lsy-6(lf) worms. (A) Cartoon of lim-6::gfp expression in wild-type and lsy-6(lf) worms. A, anterior; P, posterior; L, left; R, right. (B) Worms of indicated genotypes were scored for lim-6::gfp expression in late larval and young adult stages, n≥169. * indicates significant difference (χ², p<0.01). (C–E) Loss of mir-52 partially suppresses, while loss of mir-54/55/56 enhances, the multivulva (Muv) phenotype of let-60gf worms. (C) A wild type worm with one normal vulva, white arrow. (D) A let-60gf worm with one normal vulva, white arrow, and one ectopic vulva, black arrow. Bars represent 100 µm. (E) Synchronized L1 worms of the indicated genotype were allowed to develop at 25°C for 2–3 days and then scored as young adults for the Muv phenotype. n≥100. * indicates significant difference (χ², p<0.01). (F) Loss of mir-52 reduces the average defecation cycle time of mir-240/786 mutant worms. Average time between consecutive pBoc contractions for n≥5 worms. * indicates significant difference (student's t-test, p<0.01). Error bars indicate SEM values. (G) Loss of mir-54/55/56 enhances the embryonic lethality of mir-35 through 41 mutant worms. L4 worms of the indicated genotypes were shifted to 25° and the next day embryos from these worms were collected. After 24 hours, unhatched embryos were counted to determine the percentage of embryonic lethality (n≥148). * indicates significant difference (χ², p<0.01). (H) Loss of mir-52 modestly suppresses the resistance to levamisole of mir-1 worms. mir-52 mutants show weakly enhanced sensitivity to levamisole. * indicates significant difference compared to wild type at the indicated time point (χ², p<0.05). ** indicates significant difference compared to mir-1 at the indicated time point (χ², p<0.05).