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310 results for “Circadian clock”
Hydrobates spp. – Circadian locomotor output cycles kaput (Clock) gene poly-glutamine repeats
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Data from: The bear circadian clock doesn't 'sleep' during winter dormancy
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Data from: Developmental exposure to PCB153 (2,2’,4,4’,5,5’-hexachlorobiphenyl) alters circadian rhythms and the expression of clock and metabolic genes
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Data from: Transcription factors involved in retinogenesis are co-opted by the circadian clock following photoreceptor differentiation
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Growth hormone pulses are differentially regulated by the circadian clock gene Bmal1
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Data from: Normal vision can compensate for the loss of the circadian clock.
Circadian clocks are thought to be essential for timing the daily activity of animals, and consequently increase fitness. This view was recently challenged for clock-less fruit flies and mice that exhibited astonishingly normal activity rhythms under outdoor conditions. Compensatory mechanisms appear to enable even clock mutants to live a normal life in nature. Here, we show that gradual daily increases/decreases of light in the laboratory suffice to provoke normally timed sharp morning (M) and evening (E) activity peaks in clock-less flies. We also show that the compound eyes, but not Cryptochrome (CRY), mediate the precise timing of M and E peaks under natural-like conditions, as CRY-less flies do and eyeless flies do not show these sharp peaks independently of a functional clock. Nevertheless, the circadian clock appears critical for anticipating dusk, as well as for inhibiting sharp activity peaks during midnight. Clock-less flies only increase E activity after dusk and not before the beginning of dusk, and respond strongly to twilight exposure in the middle of the night. Furthermore, the circadian clock responds to natural-like light cycles, by slightly broadening Timeless (TIM) abundance in the clock neurons, and this effect is mediated by CRY.
Data from: Drosophila clock is required in brain pacemaker neurons to prevent premature locomotor aging independently of its circadian function
Circadian clocks control many self-sustained rhythms in physiology and behavior with approximately 24-hour periodicity. In many organisms, oxidative stress and aging negatively impact the circadian system and sleep. Conversely, loss of the clock decreases resistance to oxidative stress, and may reduce lifespan and speed up brain aging and neurodegeneration. Here we examined the effects of clock disruptions on locomotor aging and longevity in Drosophila. We found that lifespan was similarly reduced in three arrhythmic mutants (ClkAR, cyc0 and tim0) and in wild-type flies under constant light, which stops the clock. In contrast, ClkAR mutants showed significantly faster age-related locomotor deficits (as monitored by startle-induced climbing) than cyc0 and tim0, or than control flies under constant light. Reactive oxygen species accumulated more with age in ClkAR mutant brains, but this did not appear to contribute to the accelerated locomotor decline of the mutant. Clk, but not Cyc, inactivation by RNA interference in the pigment-dispersing factor (PDF)-expressing central pacemaker neurons led to similar loss of climbing performance as ClkAR. Conversely, restoring Clk function in these cells was sufficient to rescue the ClkAR locomotor phenotype, independently of behavioral rhythmicity. Accelerated locomotor decline of the ClkAR mutant required expression of the PDF receptor and correlated to an apparent loss of dopaminergic neurons in the posterior protocerebral lateral 1 (PPL1) clusters. This neuronal loss was rescued when the ClkAR mutation was placed in an apoptosis-deficient background. Impairing dopamine synthesis in a single pair of PPL1 neurons that innervate the mushroom bodies accelerated locomotor decline in otherwise wild-type flies. Our results therefore reveal a novel circadian-independent requirement for Clk in brain circadian neurons to maintain a subset of dopaminergic cells and avoid premature locomotor aging in Drosophila.
Data from: Social forces can impact the circadian clocks of cohabiting hamsters
A number of field and laboratory studies have shown that the social environment influences daily rhythms in numerous species. However, underlying mechanisms, including the circadian system's role, are not known. Obstacles to this research have been the inability to track and objectively analyse rhythms of individual animals housed together. Here, we employed temperature dataloggers to track individual body temperature rhythms of pairs of cohabiting male Syrian hamsters (Mesocricetus auratus) in constant darkness and applied a continuous wavelet transform to determine the phase of rhythm onset before, during, and after cohabitation. Cohabitation altered the predicted trajectory of rhythm onsets in 34% of individuals, representing 58% of pairs, compared to 12% of hamsters single-housed as 'virtual pair' controls. Deviation from the predicted trajectory was by a change in circadian period (t), which tended to be asymmetric—affecting one individual of the pair in nine of 11 affected pairs—with hints that dominance might play a role. These data implicate a change in the speed of the circadian clock as one mechanism whereby social factors can alter daily rhythms. Miniature dataloggers coupled with wavelet analyses should provide powerful tools for future studies investigating the principles and mechanisms mediating social influences on daily timing.
Data from: Adaptive differences in circadian clock gene expression patterns and photoperiodic diapause induction in Nasonia vitripennis
Day length (photoperiod) and temperature oscillate daily and seasonally and are important cues for season-dependent behaviour. Larval diapause of the parasitoid Nasonia vitripennis is maternally induced following a certain number of days (switch point) of a given critical photoperiod (CPP). Both the switch point and CPP follow a latitudinal cline in European N. vitripennis populations,. We previously showed that allelic frequencies of the clock gene period correlate with this diapause induction cline. Here, we report that circadian expression of four clock genes, period (per), cryptochrome-2 (cry-2), clock (clk) and cycle (cyc), oscillates as a function of photoperiod and latitude of origin in wasps from populations from the extremes of the cline. Expression amplitudes are lower in northern wasps, indicating a weaker, more plastic, clock. Northern wasps also have a later onset of activity and longer free running rhythms in constant conditions. Per RNAi caused speeding up of the circadian clock, changed the expression of other clock genes and delayed diapause in both southern and northern wasps. These results point towards adaptive latitudinal clock-gene expression differences and to a key role of per in the timing of photoperiodic diapause induction of N. vitripennis.
Data from: Differential phasing between circadian clocks in the brain and peripheral organs in humans
The daily timing of mammalian physiology is coordinated by circadian clocks throughout the body. Although measurements of clock gene expression indicate that these clocks in mice are normally in phase with each other, the situation in humans remains unclear. We used publicly available data from five studies, comprising over 1000 samples, to compare the phasing of circadian gene expression in human brain and human blood. Surprisingly, after controlling for age, clock gene expression in brain was phase-delayed by ~8.5 h relative to that of blood. We then examined clock gene expression in two additional human organs and in organs from nine other mammalian species, as well as in the suprachiasmatic nucleus (SCN). In most tissues outside the SCN, the expression of clock gene orthologs showed a phase difference of ~12 h between diurnal and nocturnal species. The exception to this pattern was human brain, whose phasing resembled that of the SCN. Our results highlight the value of a multi-tissue, multi-species meta-analysis, and have implications for our understanding of the human circadian system.
Data from: Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species
Environmental contamination is a common cause of rapid evolution. Recent work has shown that Daphnia pulex, an important freshwater species, can rapidly evolve increased tolerance to a common contaminant, sodium chloride (NaCl) road salt. While such rapid evolution can benefit organisms, allowing them to adapt to new environmental conditions, it can also be associated with unforeseen tradeoffs. Given that exposure to environmental contaminants can cause circadian disruption, we investigated whether the circadian clock was affected by evolving a tolerance to high levels of road salt. By tracking the oscillations of a putative clock gene, period, we demonstrated that D. pulex express per mRNA with approximately 20-hour oscillations under control conditions. This putative circadian rhythm was ablated in response to high levels of salinity; populations adapted to high NaCl concentrations exhibited an ablation of period oscillation. Moreover, we showed that while gene expression is increased in several other genes, including clock, actin, and Na+/K+-ATPase, upon the adaptation to high levels of salinity, per expression is unique among the genes we tracked in that it is the only gene repressed in response to salt adaptation. These results suggest that rapid evolution of salt tolerance occurs with the tradeoff of suppressed circadian function. The resultant circadian disruption may have profound consequences to individuals, populations, and aquatic food webs by affecting species interactions. In addition, our research suggests that circadian clocks may also be disrupted by the adaptation to other environmental contaminants.
thyroid hormone pathway and circadian clock genes
<p>thyroid hormone pathway and circadian clock genes</p>
Fig. 5 in Modulation of cellular circadian clocks by triterpenoids
Fig. 5. Celastrol reset the circadian clocks in U2OS, NIH3T3, and mouse tissue explants.
Fig. 2 in Modulation of cellular circadian clocks by triterpenoids
Fig. 2. Effects of corosolic acid and analogues on circadian clocks in U2OS cells.
Fig. 3. Cucurbitacin B in Modulation of cellular circadian clocks by triterpenoids
Fig. 3. Cucurbitacin B resets the circadian clocks in U2OS, NIH3T3, and mouse tissue explants.
Fig. 4 in Modulation of cellular circadian clocks by triterpenoids
Fig. 4. (continued).
Fig. 7 in Modulation of cellular circadian clocks by triterpenoids
Fig. 7. Relationship between the structures of celastrol and its analogues and clock modulation.
Fig. 2 in Modulation of cellular circadian clocks by triterpenoids
Fig. 2. (continued).
Fig. 1 in Modulation of cellular circadian clocks by triterpenoids
Fig. 1. Triterpenoids affect the circadian rhythm in U2OS cells.
Melatonin as a Circadian Clock Regulator, Neuromodulator and Myelo-protector in Adjuvant Breast Cancer Chemotherapy
ClinicalTrials.gov study NCT03205033. IPD Sharing: UNDECIDED. Countries: 0. Publications: 1.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.