Figure 2. Quantitative effects of loss of skn-1 on endoderm formation.

(A) Spectrum of skn-1(RNAi) effects across the C. elegans isolates. The effects of skn-1(RNAi) are quantified as the average percentage of arrested embryos with endoderm (y-axis). All wild isolates treated with skn-1(RNAi) resulted in 100% embryonic arrest (n > 500 embryos per replicate per isotype and at least two replicates per isotype). (B) Comparison of skn-1(RNAi) phenotype using two different gut markers (birefringent gut granules and MH33 staining of IFB-2) in five different genetic backgrounds. In all cases, no significant statistical difference was found between the two quantitative methods. Fisher’s exact test (NS p-value>0.05). (C) Comparison of skn-1(RNAi) and skn-1(zu67) effects on endoderm development in six different genetic backgrounds. For each color-coded strain, the first value is of the skn-1(RNAi) results (five replicates), while the second is the result for the skn-1(zu67) allele introgression (10 replicates). For all strains (with the exception of MY16), no significant statistical difference was found between the RNAi knockdown and corresponding skn-1(zu67) allele effects on endoderm development. Student t-test (NS p-value>0.05, * p-value<0.05).

Figure 2—figure supplement 1. High reproducibility of skn-1(RNAi) phenotypes in various C. elegans isotypes.

elegans isotypes. A minimum of two replicates were obtained, with >500 embryos per replicate (N = 3). Boxplot represents median with range bars showing upper and lower quartiles.