Table 1.

Ray development defects in lin-32 and Wnt/β-catenin asymmtery mutantsa

GenotypebRays per sideRnAs (trp-4::mCh) per sideRnBs (pkd-2::GFP) per siden (sides)
Wild-type9.0 ± 0.36.2 ± 1.57.9 ± 0.564
lin-32(tm2044Δ)2.3 ± 1.0***2.0 ± 1.0***3.3 ± 1.0***88
lin-17(n671)0.0***n.d.n.d.18
lin-17(n698)3.7 ± 2.5***7.2 ± 3.4**5.6 ± 3.5***110
lin-17(bx109)6.8 ± 2.5***6.7 ± 2.37.2 ± 3.078
lin-44(n1792)4.5 ± 2.04.0 ± 2.47.2 ± 1.636
lin-44(n1792); egl-20(n585)3.2 ± 2.0̂5.5 ± 1.6̂̂7.3 ± 1.238
lin-44(n1792); cwn-1; cwn-23.6 ± 2.15.2 ± 1.1̂7.4 ± 1.632
Control RNAi8.9 ± 0.4n.d.n.d.58
lit-1(RNAi)6.6 ± 1.7†††n.d.n.d.93
sys-1(RNAi)8.1 ± 1.1†††n.d.n.d.94
pop-1(RNAi)c3.9 ± 2.3†††n.d.n.d.100
  • n.d., Not determined. **p < 0.01, ***p < 0.001 compared with wild-type controls. *p < 0.05, **p < 0.01 compared with lin-44(n1792).

  • †††p < 0.001 compared with control RNAi.

  • aAll values are reported as mean ± SD.

  • bAll strains contain him-5(e1490) (see Materials and Methods). Except for the RNAi experiments, strains listed here also contained the transgene fsIs18.

  • cMany pop-1(RNAi) animals had large “fused” rays that could arise from either the fusion of two separate rays (as a result of a defect in ray identity specification) or the development of multiple Rnst ray structural cells from a single ray sublineage.