Fig. 4: A unique genetic pathway regulates monoallelic expression. | Nature Communications

Fig. 4: A unique genetic pathway regulates monoallelic expression.

From: Maternal histone methyltransferases antagonistically regulate autosomal random monoallelic expression (aRMAE) in C. elegans

Fig. 4

For (a–h), scatter plots (left panel) and boxplots (right panel) are all from intestine cells from animals with indicated mutations or RNAi. Top of boxplot is 75th percentile, bottom of box is 25th percentile, line is median, top and bottom error bars are 90th and 10th percentile, respectively, and dots are 95th and 5th percentile. a cec-4(RNAi) had no significant effect on aRMAE, (0.00467 vs control 0.00371); P > 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, N = 207 cells for control, N = 210 cells for cec-4(RNAi), three independent experiments. b lem-2(RNAi) had no significant effect on aRMAE, (0.00624 vs control 0.00371); P > 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, N = 207 cells for control, N = 210 cells for lem-2(RNAi), three independent experiments. c arle-14 negatively regulates aRMAE, with a significantly higher median intrinsic noise of 0.0110 for arle-14(RNAi) compared to 0.00371 for control animals; P < 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, N = 207 cells for control, N = 210 cells for arle-14(RNAi), three independent experiments. d lin-65 is a strong negative regulator of aRMAE, with a significantly higher intrinsic of 0.0110 for lin-65(RNAi) vs 0.00371 for controls, P < 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, 207 cells for each group, three independent experiments. e lin-61 is a strong positive regulator of aRMAE. lin-61(RNAi) animals had a significantly lower intrinsic noise of 0.00105 compared to 0.00371 for control animals; P < 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, N = 207 cells for control, N = 210 cells for lin-61(RNAi), three independent experiments. f similar to lin-61, set-25 is also a strong positive regulator of aRMAE. set-25(RNAi) animals had a significantly lower intrinsic noise of 0.00109 compared to 0.00371 for control animals; P < 0.05, Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method, N = 207 cells for control, N = 208 cells for set-25(RNAi), three independent experiments. g The enhanced aRMAE phenotype in met-2(null) animals is dependent upon lin-61. The met-2(null);lin-61(RNAi) animals had a significantly lower intrinsic noise of 0.00160 compared to 0.254 for met-2(null) animals; P < 0.05 Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method for multiple comparison, N = 199 for met-2(null), N = 210 for met-2(null);lin-61(RNAi), three independent experiments. h Similar to (g), the enhanced aRMAE phenotype in met-2(null) animals is dependent upon set-25. The met-2(null);set-25(RNAi) animals had a significantly lower intrinsic noise of 0.00237 compared to 0.254 for met-2(null) animals; P < 0.05 Kruskal–Wallis One Way Analysis of Variance on Ranks followed by Dunn’s Method for multiple comparison, N = 199 cells for met-2(null), N = 204 cells for met-2(null);set-25(RNAi), three independent experiments. i Merged confocal microscope images of met-2(null) control, met-2(null);lin-61(RNAi), and met-2(null);set-25(RNAi) animals with a 10 micrometer white scale bar inset in the bottom left of the control animal. j Summary of the genetic pathway controlling aRMAE from the results. Additional statistical and genetic comparisons are shown in Supporting Information Section 2; see Supplemental Fig. 3 for additional genetic tests.

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