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The 2017 Nobel Prize in Physiology or Medicine was awarded to Jeffrey C. Hall, Michael Rosbash and Michael W. Young for their elucidation of the molecular mechanisms controlling circadian rhythm. Their pioneering work in Drosophila uncovered the internal oscillators, or clocks, that synchronise cellular metabolism and organismal behaviour to the light/dark cycle to generate biological rhythms with 24 hour periodicity.
Genetic and biochemical assays reveal that carbon monoxide produced by heme catabolism influences circadian rhythm in mammals by altering the activity of transcription factor CLOCK–BMAL1 at clock-gene targets.
The effect of the liver clock is modified by food entrainment via Bmal1/Clock core machinery. Here the authors show that insulin promotes postprandial Akt-dependent phosphorylation of Bmal1, resulting in association with 14-3-3 and Bmal1 shuttling out of the nucleus, thereby disrupting Bmal1 transcriptional effects on the clock.
This study finds that mice's biological clocks are permanently influenced by the seasonal photoperiod at and after birth. In mice raised under summer-like light periods, rhythmic gene expression in the suprachiasmatic nucleus was tightly correlated with lights-off under both summer- and winter-like cycles. In 'winter-born' mice, these rhythms were tightly correlated only under winter-like light cycles.
Circadian rhythms and related behaviours vary across individuals. Here, a large genome-wide association study reveals common single nucleotide variants influencing whether an individual reports as being a ‘morning person’ by identifying 15 significant loci, including 7 near known circadian genes.
Trypanosoma brucei, which is responsible for human sleeping sickness, has an intrinsic circadian clock that regulates metabolism and influences drug sensitivity.
New data show that Clock–Bmal1, the central transcriptional activator that drives expression of circadian target genes, also recruits the Ddb1–Cullin-4 ubiquitin ligase to clock promoters to enhance the subsequent binding of the feedback repressors that generate the circadian periodicity of gene expression.
Maillo et al. show that in hepatocytes ER stress upregulates CPEB4 through the UPR and circadian clock, leading to CPEB4-mediated translation for mitochondrial and ER homeostasis. CPEB4 loss leads to ageing- and high fat diet-induced liver steatosis.
The evening complex coordinates plant growth and environmental signalling with the circadian clock. Here, a comprehensive dataset of direct transcriptional targets of the evening complex uncovers a high-quality global regulatory network.
Genetic deletion of HDAC3, a circadian epigenome regulator, specifically in skeletal muscle alters amino acid metabolism, leading to increased muscle endurance but at the cost of whole-body insulin resistance.
Accumulating evidence suggests that microRNAs play a role in circadian regulation. Here the authors show that in theDrosophila brain, mir-92a suppresses the excitability of PDF neurons—key circadian pacemaker cells in Drosophila—via inhibiting the translation of its target sirt2.
This study characterizes a subset of clock neurons known as large lateral-ventral neurons and their dopaminergic/octopaminergic input circuitry in balancing light-mediated wakefulness in Drosophila.
CLOCK (CLK) is essential for the development and maintenance of circadian rhythms in Drosophila. Here, the authors show that Clk mRNA is regulated by miRNA bantam, and deletion of bantambinding site leads to stochastic CLK-driven transcription and development of the circadian neurons.
This study uses a new method of profiling cell type–specific gene expression to identify genes expressed in fruitfly clock neurons. Such profiling yields two novel circadian genes, in separate sets of clock neurons and with differing circadian functions.