Dataset Information

Rapid Response and Slow Recovery of the H3K4me3 Epigenomic Marker in the Liver After a Light-Mediated Phase Advance of the Circadian Clock

ABSTRACT: Mammalian tissues display circadian rhythms in which transcription levels rise and fall throughout a 24-hour day. These rhythms include histone modifications. Here we asked whether an advance of the light-dark cycle could alter rhythms in the liver epigenome at the H3K4me3 (trimethylation of lysine 4 on histone 3) modification, which is found at active and poised gene promoters. H3K4me3 levels were first measured at 4-time points (Zeitgeber Time [ZT] 3, 8, 15, and 20) during a normal 12L:12D light:dark cycle. Peak levels were observed during the early dark phase at ZT15, and dropped to low levels around lights-on (ZT0) between ZT20 and ZT3. A six-hour phase advance at ZT18 (new lights-on after only 6 h of darkness) led to a transient extension of peak H3K4me3 levels. Although locomotor activity re-entrained within a week after the phase advance, H3K4me3 rhythms failed to do so with peak levels remaining in the light phase at the one-week recovery time point. Eight weekly phase advances, with one-week recovery times between each phase advance, also led to disruption of the liver circadian epigenome. A model to explain these results is offered.

ORGANISM(S): Mus musculus

PROVIDER: GSE108481 | GEO | 2018/12/01

REPOSITORIES: GEO

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Project description:Living organisms detect seasonal changes in day length (photoperiod), and alter their physiological functions accordingly, to fit seasonal environmental changes. This photoperiodic system is implicated in seasonal affective disorders and the season-associated symptoms observed in bipolar disease and schizophrenia. Thyroid-stimulating hormone beta subunit (Tshb), induced in the pars tuberalis (PT), plays a key role in the pathway that regulates animal photoperiodism. However, the upstream inducers of Tshb expression remain unknown. Here we show that late-night light stimulation acutely triggers the Eya3-Six1 pathway, which directly induces Tshb expression. Using melatonin-proficient CBA/N mice, which preserve the photoperiodic Tshb-expression response, we performed a genome-wide expression analysis of the PT under chronic short-day and long-day conditions. These data comprehensively identified long-day and short-day genes, and indicated that late-night light stimulation induces long-day genes. We verified this by advancing and extending the light period by 8 hours, which acutely induced Tshb expression, within one day. In a genome-wide expression analysis under this condition, we searched for candidate upstream genes by looking for expression that preceded Tshb’s, and identified Eya3 gene. These results elucidate the comprehensive transcriptional photoperiodic response in the PT, revealing the complex regulation of Tshb expression and unexpectedly rapid response to light changes in the mammalian photoperiodic system. Mice were separated into 2 groups. One group was maintained under the short-day conditions (light: dark = 8 h:16 h, ZT0 = lights on, ZT8 = lights off, 400 lux) and the other was housed under long-day conditions (light:dark = 16 h:8 h, ZT0 = lights on, ZT16 = lights off, 400 lux) for 2 weeks. The PTs of both groups were retrieved every 4 h for 1 day (6 time points for each group), starting at ZT0. For the experiments performed during the first day of the long-day conditions, we applied two different conditions, following 3 weeks under short-day conditions. In one, the light-onset was advanced by 8 hours (advance condition), and in the other, the dark period was delayed by 8 hours (delay condition). PTs from both groups were obtained every 4 h for 1 day, starting at the lights-on time. (Lights on for the advance condition was ZT16 as defined by the short-day condition. Lights on for the delay condition was ZT0). We sampled 25 mice at each time point. This whole procedure was repeated twice (n = 2) to obtain experimental replicates.

Dataset Information

Rapid Response and Slow Recovery of the H3K4me3 Epigenomic Marker in the Liver After a Light-Mediated Phase Advance of the Circadian Clock

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