Figure 4. TIP60-deficiency evokes a circadian phenotype in mice and disrupts rhythmic clock gene expression in the SCN and in MEFs.
(A) Double-plotted actograms of control (Syt10Cre/+Tip60+/+) and mutant (Syt10Cre/+Tip60 fl/-, Syt10Cre/Cre Tip60fl/-) mice under 12 hr:12 hr light-dark and constant darkness conditions. Gray shadings indicate dark phases. (B) Free-running periods determined by χ2 periodogram analysis. AR: arrhythmic (***p<0.001, one-way ANOVA with Bonferroni post-test). (C) TIP60-immunoreactivity (ir) in the SCN of control (Syt10Cre/+Tip60+/+) and arrhythmic mutant (Syt10Cre/+Tip60 fl/-) mice. (D) Densitometric quantification of clock gene mRNA expression from radioactive in situ hybridization analysis of control (Syt10Cre/+Tip60+/+; black) and mutant (Syt10Cre/+Tip60 fl/-; gray) SCN sections (n = 3; two-way ANOVA, see Supplementary file 1). (E) Bioluminescence recordings of synchronized Tip60fl/-; Bmal1-LUC MEFs transduced with AdGFP (black) or AdCre (gray) (n = 4). (F) mRNA expression analysis of Dex synchronized Tip60fl/- MEFs transduced with either AdGFP (black) or AdCre (gray) (n = 3; two-way ANOVA, see Supplementary file 1). All data are shown as mean ± SD.