Project description:With the exception of latitudes close to the equator, seasonal variation in light hours can change dramatically between summer and winter. Yet, investigations into the interplay between energy metabolism and circadian rhythms typically use a 12 h light:12 h dark photoperiod corresponding to light duration at the equator. Here, we hypothesised that altering seasonal photoperiod affects both rhythmicity of peripheral tissue clocks as well as processes involved in energy storage and utilisation. Male mice were housed at one of three photoperiods representing light hours in summer, winter and the equinox. Mice housed at a winter photoperiod exhibited an increase in the amplitude of rhythmic lipid metabolism and a modest reduction in fat mass and liver triglyceride content. Comparing melatonin proficient and deficient mice, we provide evidence that the effect of seasonal light on energy metabolism is largely driven by differences in the rhythmicity of food intake, but not melatonin. Our results show that seasonal light impacts energy metabolism in mice and suggest that these effects are partly driven by modulating the timing of eating. Our work sets a course to integrate seasonal light duration in future circadian biology studies.
Project description:Organisms have adapted to the changing environmental conditions within the 24h cycle of the day by temporally segregating tissue physiology to the optimal time of the day. On the cellular level temporal segregation of physiological processes is established by the circadian clock, a Bmal1 dependent transcriptional oscillator network. The circadian clocks within individual cells of a tissue are synchronised by environmental signals, mainly light, in order to reach temporally segregated physiology on the tissue level. However, how light mediated synchronisation of peripheral tissue clocks is achieved mechanistically and whether circadian clocks in different organs are autonomous or interact with each other to achieve rhythmicity is unknown. Here we report that light can synchronise core circadian clocks in two peripheral tissues, the epidermis and liver hepatocytes, even in the complete absence of functional clocks in any other tissue within the whole organism. On the other hand, tissue extrinsic circadian clock rhythmicity is necessary to retain rhythmicity of the epidermal clock in the absence of light, proving for the first time that the circadian clockwork acts as a memory of time for the synchronisation of peripheral clocks in the absence of external entrainment signals. Furthermore, we find that tissue intrinsic Bmal1 is an important regulator of the epidermal differentiation process whose deregulation leads to a premature aging like phenotype of the epidermis. Thus, our results establish a new model for the segregation of peripheral tissue physiology whereby the synchronisation of peripheral clocks is acquired by the interaction of a light dependent but circadian clock independent pathway with circadian clockwork dependent cues.
Project description:Efficiency and reliability of energy systems in urban districts with seasonal energy storage in aquifers (Aquifer Thermal Energy Storage ATES Berlin)
Project description:Organisms have adapted to the changing environmental conditions within the 24h cycle of the day by temporally segregating tissue physiology to the optimal time of the day. On the cellular level temporal segregation of physiological processes is established by the circadian clock, a Bmal1 dependent transcriptional oscillator network. The circadian clocks within individual cells of a tissue are synchronised by environmental signals, mainly light, in order to reach temporally segregated physiology on the tissue level. However, how light mediated synchronisation of peripheral tissue clocks is achieved mechanistically and whether circadian clocks in different organs are autonomous or interact with each other to achieve rhythmicity is unknown. Here we report that light can synchronise core circadian clocks in two peripheral tissues, the epidermis and liver hepatocytes, even in the complete absence of functional clocks in any other tissue within the whole organism. On the other hand, tissue extrinsic circadian clock rhythmicity is necessary to retain rhythmicity of the epidermal clock in the absence of light, proving for the first time that the circadian clockwork acts as a memory of time for the synchronisation of peripheral clocks in the absence of external entrainment signals. Furthermore, we find that tissue intrinsic Bmal1 is an important regulator of the epidermal differentiation process whose deregulation leads to a premature aging like phenotype of the epidermis. Thus, our results establish a new model for the segregation of peripheral tissue physiology whereby the synchronisation of peripheral clocks is acquired by the interaction of a light dependent but circadian clock independent pathway with circadian clockwork dependent cues.
Project description:The neuroendocrine regulation of seasonal energy homeostasis and rheostasis are widely studied. However, the molecular pathways underlying tissue-specific adaptations remain poorly described. We conducted an experiment to examine long-term rheostatic changes in energy stability using the well-characterized photoperiodic response of the Japanese quail. We exposed quails to photoperiodic transitions simulating the annual photic cycle and examined the morphology and fat deposition in liver, and white adipose tissue. To identify molecular substrates during the vernal transition in lipid accumulation, we conducted transcriptomic analyses of white adipose and liver tissues. We identified transcripts involved in adipocyte growth (Cysteine Rich Angiogenic Inducer 61, Very Low Density Lipoprotein Receptor) and obesity-linked disease resistance (Insulin-Like Growth Factor Binding Protein 2, Apolipoprotein D) increase expression in anticipation of body mass gain. In the liver, under long photoperiods, transcripts involved in fatty acid (FA) synthesis (Fatty Acid Synthase, Fatty Acid Desaturase 2) were down-regulated. Parallel upregulation of hepatic Fatty Acid Translocase and Pyruvate Dehydrogenase Kinase 4 expression suggests increased circulatory FA uptake and a switch from glucose to FA utilization. Overall, we have identified tissue-specific biochemical and molecular changes that drive photoperiod-induced adipogenesis in quails. These findings can be use to determine conserved pathways that enable animals to accumulate fat without developing metabolic diseases.
Project description:The mammalian circadian system consists of a central clock in the brain that synchronizes clocks in peripheral tissues. While the hierarchy between the central and peripheral clocks is well established, peripheral clocks are largely viewed as a group and little is known regarding their specificity and functional organization. We employed feeding paradigms in conjunction with liver-specific clock-deficient murine model to map disparities and potential interactions between peripheral clocks. We found that peripheral clocks largely differ in their response to feeding-time. In view of its prominent role in nutrient processing, we hypothesized that the liver-clock instigate the response of peripheral clocks to feeding. Although the liver-clock did not affect the rhythmicity of clocks in other peripheral tissues, it strongly modulated their transcriptional rhythmicity upon daytime feeding. Overall, our findings suggest a role for the liver-clock in buffering feeding-related signals that affect rhythmicity of other peripheral tissues upon nutrient challenge, irrespective of their clocks.
Project description:In this study, we used RNA sequencing to interrogate how muscle and liver autonomous clocks influence the circadian transcriptome across these two organs.