Skip to main content
Fig. 5 | Genome Biology

Fig. 5

From: cis-regulatory variation modulates susceptibility to enteric infection in the Drosophila genetic reference panel

Fig. 5

Broad binding affinity and ntc expression is lowered for the alternate allele. a Top panel: schematic of the ntc gene with specific annotations: cis-eQTLs around the ntc locus, and their overlap with predicted TF binding sites (TFBS). TFBS prediction was done using FIMO [70] and motifs from the Fly Factor Survey [71] and OnTheFly [72] databases. The expression fold change of ntc by resistance class and two of those alleles (termed the broad/daughterless allele (left panel), and the relish allele (right panel)) is plotted, as well as the survival percentage of 140 DGRP lines [31]. Green and red boxplots represent resistant and susceptible DGRP lines, respectively. b Measure of the binding affinity between Broad and the reference or alternate allele as measured by MITOMI [73, 74] in three different replicates. c Repartition of lines in the round robin scheme based on reference or alternate broad TFBS alleles. d Ratios of read count mapping to the alternate over the reference allele reveal no difference in control condition (t-test, p value = 0.21) but is significant in the infected condition (t-test p value = 0.04). e Proposed model of ntc-mediated variation in gut immunocompetence: an enteric immune challenge increases ntc expression, while Broad acts as a repressor of ntc expression. The SNP in the Broad binding site decreases the binding affinity for Broad and thus the extent of ntc repression, resulting in greater ntc expression, which in turn increases DiptA expression and overall gut immunocompetence

Back to article page