Fig. 3
From: Misalignment with the external light environment drives metabolic and cardiac dysfunction
Robust circadian rhythms in clock gene expression are maintained in non-24 h LD housed mice. Representative brain sections a and quantification b of radioactive in situ hybridisation for Per1 expression in the SCN from mice housed in 24 h (black) or 22.5 h (red) conditions for 17 week. c Circulating corticosterone profiles were delayed relative to the LD cycle in mice housed under or 22.5 h conditions. d Acrophase analysis of Per1 and corticosterone rhythms in 24 and 22.5 h housed mice reveals consistent phase delay. e Profiling of clock gene expression in peripheral tissues of mice housed in 24 or 22.5 h LD conditions for 17 weeks. f Acrophase analyses across genes and tissues (plotted relative to respective light cycle) demonstrates that synchronisation both within and across tissue clocks is maintained in non-24 h LD conditions. All data plotted mean ± SEM relative to the respective light cycle (24 or 22.5 h) and normalised to ZT0 of the 24 h LD group (n = 4/time-point/group). ∗Significant (p < 0.05) difference in phase between 24 and 22.5 h profiles; a significant difference in amplitude or mesor between 24 and 22.5 h LD conditions (sinusoidal waveform fits with F tests for shared characteristics). Scale bar in a = 3 mm
