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. 2020 Aug 21;2(2):fcaa133. doi: 10.1093/braincomms/fcaa133

Figure 6.

Figure 6

Haploinsufficiency of TBK1 shifts the spinal inflammatory transcriptome towards ageing in young mice. (A) Unbiased hierarchical cluster analysis (average linkage) on all 800 genes of the neuroinflammation panel in the spinal cord of young and aged wt and Tbk1+/− mice. Cluster analysis completely separates young from old mice and wt from Tbk1+/− mice at the age of 4 months. (B) The microglia-specific gene score shows an age-dependent increase that is independent of Tbk1. (C) The astrocyte-specific gene score is increased in Tbk1+/− mice compared to wt siblings at 4 but not at 22 months. The astroglia gene score is age-dependently increased in wt mice. (D) The oligodendrocyte-specific gene score is not affected by genotype or age. (E) The endothelial-specific gene score is increased in Tbk1+/− mice compared to wt siblings at 4 but not at 22 months. (F) Volcano plot showing 5 (including Tbk1) out of 800 genes after FDR correction for multiple testing differently regulated when comparing both genotypes at age 4 months. Horizontal line indicates threshold for FDR (0.05). (G) A principal component analysis of the same 800 gene panel shows a shift of the transcriptomic inflammatory profile of young Tbk1+/− mice towards that of old ones. (H) Positive correlation of age-associated changes with changes caused by Tbk1 haploinsufficiency in young mice, based on the 219 genes significantly altered by ageing. (B)–(E) Graphs have been analysed by two-way ANOVA followed by Tukey’s multiple comparisons. All bar graphs are shown as mean ± SEM. *P < 0.05; **P < 0.01;***P < 0.001. N = 5.