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. Author manuscript; available in PMC: 2022 Jan 8.
Published in final edited form as: Nat Aging. 2021 Jul 8;1(7):585–597. doi: 10.1038/s43587-021-00072-0

Fig. 2 |. AP1 activation is sustained and is severity-dependent.

Fig. 2 |

a, AP1 activation was assessed in TREdsRed transgenic flies, with dsRed driven by 4X AP1 motifs. Right, 15 dpi survival of TREdsRed flies injured with sham (black), mild (35% head compression), or severe (45% head compression) dTBI (n = 100 per condition; sham vs mild dTBI: p = 0.00011, sham vs severe dTBI: p < 2e-16, mild vs severe dTBI: p = 1.6e-7, Kaplan-Meier analysis with log-rank comparison). b, Representative z-stacked whole mount brains at 1 dpi across injury conditions. Scale bar, 100μm. c, Quantification of dsRed immunofluorescence in whole mount brains throughout the post-injury period (each point = 1 brain; n = 14–19 brains per condition/time pooled examined over two independent experiments; p = 3.33e-09, two-way ANOVA with Tukey’s test). d, Mean relative expression of dsRed mRNA by RT-qPCR at 1, 7, and 15 dpi between injury conditions (each point = 1 biological replicate of 9 brains; n = 6 biological replicates per condition; Kruskal–Wallis test with Dunn’s multiple comparison test and Holm adjustment). See Extended Data Fig. 2b for additional AP1 target genes. Statistical annotations are ****p<0.0001, ***p<0.001, **p<0.01, *p<0.05, -p<0.10. All statistical tests were two-sided where applicable. For full statistical reporting, including exact p-values, see Source Data Fig. 2. Scale bar 100μm. Color code for injury in a and b.