Fig. 3
From: Inferring cell-type-specific causal gene regulatory networks during human neurogenesis
Biological and technical features predicting causality. a Percent variance in gene expression explained by chromatin accessibility (r2(Y,M)) in X-M-Y triplets supporting causal forward model versus independence in progenitors (upper, purple) and neurons (lower, green). Unpaired t-test p-value is shown. b Absolute distance of variants relative to TSS of the genes for X-M-Y triplets supporting causal forward model versus independence in progenitors (upper, purple) and neurons (lower, green). Unpaired t-test p-value is shown. c Distribution of variants located within gene promoter (within + / − 2 kb window from gene TSS) within X-M-Y triplets supporting causal forward model versus independence in progenitors (upper, purple) and neurons (lower, green). Chi-square test p-value is shown. d Number of testable variants detected to disrupt TF binding motifs via motifbreakR in X-M-Y triplets supporting causal forward model versus independence in progenitors (upper, purple) and neurons (lower, green). Chi-square test p-value is shown. e Number of testable variants (either variant itself or LD proxy) showed allele-specific chromatin accessibility (ASCA) in X-M-Y triplets supporting causal forward model versus independence in progenitors (upper, purple) and neurons (lower, green). Chi-square test p-value is shown