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Andreatta, G., & Tessmar-Raible, K. (2020). The still dark side of the moon: molecular mechanisms of lunar-controlled rhythms and clocks. J Mol Biol, in press.
Abstract: Starting with the beginning of the last century, a multitude of scientific studies has documented that the lunar cycle times behaviors and physiology in many organisms. It is plausible that even the first life forms adapted to the different rhythms controlled by the moon. Consistently, many marine species exhibit lunar rhythms, and also the number of documented “lunar-rhythmic” terrestrial species is increasing. Organisms follow diverse lunar geophysical/astronomical rhythms, which differ significantly in terms of period length: from hours (circalunidian and circatidal rhythms) to days (circasemilunar and circalunar cycles). Evidence for internal circatital and circalunar oscillators exists for a range of species based on past behavioral studies, but those species with well-documented behaviorally free-running lunar rhythms are not typically used for molecular studies. Thus, the underlying molecular mechanisms are largely obscure: the dark side of the moon. Here we review findings which start to connect molecular pathways with moon-controlled physiology and behaviors. The present data indicate connections between metabolic/endocrine pathways and moon-controlled rhythms, as well as interactions between circadian and circatidal/circalunar rhythms. Moreover, recent high-throughput analyses provide useful leads towards pathways, as well as molecular markers. However, for each interpretation it is important to carefully consider the – partly substantially differing – conditions used in each experimental paradigm. In the future, it will be important to use lab experiments to delineate the specific mechanisms of the different solar- and lunar-controlled rhythms, but to also start integrating them together, as life has evolved equally long under rhythms of both sun and moon.
Keywords: Review; Animals; Hormones; Lunar rhythms; Physiology; Proteome; Transcriptome
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Barclay, J. L., Husse, J., Bode, B., Naujokat, N., Meyer-Kovac, J., Schmid, S. M., et al. (2012). Circadian desynchrony promotes metabolic disruption in a mouse model of shiftwork. PLoS One, 7(5), e37150.
Abstract: Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.
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van der Burght, B. W., Hansen, M., Olsen, J., Zhou, J., Wu, Y., Nissen, M. H., et al. (2013). Early changes in gene expression induced by blue light irradiation of A2E-laden retinal pigment epithelial cells. Acta Ophthalmol, 91(7), e537–45.
Abstract: PURPOSE: Accumulation of bisretinoids as lipofuscin in retinal pigment epithelial (RPE) cells is implicated in the pathogenesis of some blinding diseases including age-related macular degeneration (AMD). To identify genes whose expression may change under conditions of bisretinoid accumulation, we investigated the differential gene expression in RPE cells that had accumulated the lipofuscin fluorophore A2E and were exposed to blue light (430 nm). METHODS: A2E-laden RPE cells were exposed to blue light (A2E/430 nm) at various time intervals. Cell death was quantified using Dead Red staining, and RNA levels for the entire genome was determined using DNA microarrays (Affymetrix GeneChip Human Genome 2.0 Plus). Array results for selected genes were confirmed by real-time reverse-transcriptase polymerase chain reaction. RESULTS: Principal component analysis revealed that the A2E-laden RPE cells irradiated with blue light were clearly distinguishable from the control samples. We found differential regulation of genes belonging to the following functional groups: transcription factors, stress response, apoptosis and immune response. Among the last mentioned were downregulation of four genes that coded for proteins that have an inhibitory effect on the complement cascade: (complement factor H, complement factor H-related 1, complement factor I and vitronectin) and of two belonging to the classical pathway (complement component 1, s subcomponent and complement component 1, r subcomponent). CONCLUSION: This study demonstrates that blue light irradiation of A2E-laden RPE cells can alter the transcription of genes belonging to different functional pathways including stress response, apoptosis and the immune response. We suggest that these molecules may be associated to the pathogenesis of AMD and can potentially serve as future therapeutic targets.
Keywords: Apoptosis; Cell Line; Cell Survival; Gene Expression Regulation/*physiology; Humans; Light; Lipofuscin/genetics; Oligonucleotide Array Sequence Analysis; Principal Component Analysis; Pyridinium Compounds; RNA, Messenger/genetics; Real-Time Polymerase Chain Reaction; Retinal Pigment Epithelium/metabolism/pathology/*radiation effects; Retinoids/*genetics; Transcriptome; A2e; age-related macular degeneration; apoptosis; complement cascade; gene expression; retinal pigment epithelial cells; blue light; retinal pigment epithelial; epigenetics
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