Fig. 4: Microbiota drive RIPK1 kinase and TRADD co-dependent intestinal pathology in adult Tak1 ^tamIEC-KO mice.

a Kaplan–Meier survival curves of the indicated genotypes. ABX was pretreated for 14 days before and through tamoxifen injection of the mice with indicated genotypes until sacrificed. Survival data for Tak1^tamIEC-KO Ripk1^D138N/D138N mice from Fig. 1k were included for comparison. b Relative body weight of the mice with indicated genotypes at 7 dpi. The body weight of each mouse was normalized to the weight of day 0. Body weight data for Tak1^fl/fl Ripk1^D138N/D138N and Tak1^tamIEC-KO Ripk1^D138N/D138N mice at 7 dpi from Fig. 1l were included for comparison. c, d Representative images of colon sections from the mice at 7 dpi with indicated genotypes stained with H&E or immunostained for CC3 (c). Graphs showed the CC3⁺ signals in the colon of the mice with indicated genotypes (d). CC3⁺ signals for Tak1^fl/fl Ripk1^D138N/D138N mice and Tak1^tamIEC-KO Ripk1^D138N/D138N mice from Fig. 1s were included for comparison. e PCA on RNA-seq data from the colon of the mice with indicated genotypes at 7 dpi. PCA was based on genes differentially expressed between Tak1^fl/fl Ripk1^D138N/D138N mice and Tak1^tamIEC-KO Ripk1^D138N/D138N mice (cut-off: log2|fold change | ≥1, p ≤ 0.05). f GO analysis of genes upregulated in the colon of Tak1^tamIEC-KO Ripk1^D138N/D138N mice in TRADD-dependent fashion. g The mRNA levels of inflammatory cytokines in the colon of the mice with indicated genotypes at 7 dpi were measured by qRT-PCR. Scale bar, 150 μm. Each dot represented one mouse. The results were shown as mean ± SEM. An unpaired two-tailed t-test was performed.