Fig. 3

Ppa-nhr-10 mutations do not affect mouth morphology and only weakly affects mouth-form plasticity. (A) Gene model of Ppa-nhr-10 and frameshift alleles which lead to early truncation of the ligand-binding domain. e = exon. (B) Ratio of predatory (Eu) and bacterivorous (St) animals in the population. Worms were raised and scored on agar plates with E. coli OP50 as a food source. Three biological replicates were obtained (n = 3) and 150 worms of each strain were scored per replicate. Significant differences are indicated in black, non-significant ones in gray. Z-scores and P-values were derived from a two-tailed PERMANOVA with null model residual randomization (RRPP). Bars represent mean values across all replicates; error bars indicate ± 1 standard error of the mean. (C) Geometric morphometric analysis of form differences in the nematode mouths. The PCA plot shows the distribution of mouth morphologies of individual worms in a form space. Note that the ranges of morphological variation (outlined by convex hulls) in Ppa-nhr-10 mutant strains completely overlap with the wild-type range of morphological variation. (D) Unsupervised (model-based) clustering reveals that all 144 individuals belong to a single morphological cluster, demonstrating that mutant worms cannot be differentiated from wild-type worms based on mouth morphology. Only predatory (Eu) animals were used for the analyses in (C) and (D)