scholarly journals The Nitrate Reductase Circadian System. The Central Clock Dogma Contra Multiple Oscillatory Feedback Loops: Fig. 1.

2001 ◽  
Vol 125 (4) ◽  
pp. 1554-1557 ◽  
Author(s):  
Cathrine Lillo ◽  
Christian Meyer ◽  
Peter Ruoff
2018 ◽  
Vol 179 (1) ◽  
pp. R1-R18 ◽  
Author(s):  
Ayrton Custodio Moreira ◽  
Sonir Rauber Antonini ◽  
Margaret de Castro

The circadian rhythm of glucocorticoids has long been recognised within the last 75 years. Since the beginning, researchers have sought to identify basic mechanisms underlying the origin and emergence of the corticosteroid circadian rhythmicity among mammals. Accordingly, Young, Hall and Rosbash, laureates of the 2017 Nobel Prize in Physiology or Medicine, as well as Takahashi’s group among others, have characterised the molecular cogwheels of the circadian system, describing interlocking transcription/translation feedback loops essential for normal circadian rhythms. Plasma glucocorticoid circadian variation depends on the expression of intrinsic clock genes within the anatomic components of the hypothalamic–pituitary–adrenal axis, which are organised in a hierarchical manner. This review presents a general overview of the glucocorticoid circadian clock mechanisms, highlighting the ontogeny of the pituitary–adrenal axis diurnal rhythmicity as well as the involvement of circadian rhythm abnormalities in the physiopathology and diagnosis of Cushing’s disease.


2011 ◽  
Vol 49 ◽  
pp. 1-17 ◽  
Author(s):  
Hugh D. Piggins ◽  
Clare Guilding

Humans and other mammals exhibit a remarkable array of cyclical changes in physiology and behaviour. These are often synchronized to the changing environmental light–dark cycle and persist in constant conditions. Such circadian rhythms are controlled by an endogenous clock, located in the suprachiasmatic nuclei of the hypothalamus. This structure and its cells have unique properties, and some of these are reviewed to highlight how this central clock controls and sculpts our daily activities.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Zohar Ben-Moshe ◽  
Nicholas S. Foulkes ◽  
Yoav Gothilf

The zebrafish constitutes a powerful model organism with unique advantages for investigating the vertebrate circadian timing system and its regulation by light. In particular, the remarkably early and rapid development of the zebrafish circadian system has facilitated exploring the factors that control the onset of circadian clock function during embryogenesis. Here, we review our understanding of the molecular basis underlying functional development of the central clock in the zebrafish pineal gland. Furthermore, we examine how the directly light-entrainable clocks in zebrafish cell lines have facilitated unravelling the general mechanisms underlying light-induced clock gene expression. Finally, we summarize how analysis of the light-induced transcriptome and miRNome of the zebrafish pineal gland has provided insight into the regulation of the circadian system by light, including the involvement of microRNAs in shaping the kinetics of light- and clock-regulated mRNA expression. The relative contributions of the pineal gland central clock and the distributed peripheral oscillators to the synchronization of circadian rhythms at the whole animal level are a crucial question that still remains to be elucidated in the zebrafish model.


2020 ◽  
Author(s):  
Anna N. King ◽  
Jessica E. Schwarz ◽  
Cynthia T. Hsu ◽  
Annika F. Barber ◽  
Amita Sehgal

AbstractSleep is controlled by homeostatic mechanisms, which drive sleep following periods of wakefulness, and a circadian clock, which regulates sleep timing in a daily cycle. Homeostatic sleep drive sometimes overrides the clock, such that recovery sleep after deprivation occurs outside the normal circadian rest period. However, mechanisms underlying this effect are unknown. We find that sleep-promoting dorsal fan-shaped body (dFB) neurons, effectors of homeostatic sleep in Drosophila, are presynaptic to hugin+ neurons, previously identified as circadian output neurons regulating locomotor activity rhythms. Sleep deprivation decreases hugin+ neuronal activity, which likely suppresses circadian control to promote recovery sleep driven by dFB neurons. Indeed, removal of hugin+ neurons increases sleep-promoting effects of dFB neurons. Trans-synaptic mapping reveals that hugin+ neurons feed back onto s-LNv central clock neurons, which also show Hugin-dependent decreased activity upon sleep loss. These findings identify a circuit-based mechanism through which sleep drive modulates the circadian system to promote recovery sleep following deprivation.


2001 ◽  
Vol 356 (1415) ◽  
pp. 1687-1696 ◽  
Author(s):  
Till Roenneberg ◽  
Martha Merrow

After approximately 50 years of circadian research, especially in selected circadian model systems ( Drosophila, Neurospora, Gonyaulax and, more recently, cyanobacteria and mammals), we appreciate the enormous complexity of the circadian programme in organisms and cells, as well as in physiological and molecular circuits. Many of our insights into this complexity stem from experimental reductionism that goes as far as testing the interaction of molecular clock components in heterologous systems or in vitro . The results of this enormous endeavour show circadian systems that involve several oscillators, multiple input pathways and feedback loops that contribute to specific circadian qualities but not necessarily to the generation of circadian rhythmicity. For a full appreciation of the circadian programme, the results from different levels of the system eventually have to be put into the context of the organism as a whole and its specific temporal environment. This review summarizes some of the complexities found at the level of organisms, cells and molecules, and highlights similar strategies that apparently solve similar problems at the different levels of the circadian system.


2020 ◽  
Author(s):  
Cristina Sandu ◽  
Prapimpun Wongchitrat ◽  
Nadia Mazzaro ◽  
Catherine Jaeger ◽  
Hugo Calligaro ◽  
...  

AbstractMultiple circadian clocks dynamically regulate mammalian physiology. In retina, rhythmic gene expression serves to align vision and tissue homeostasis with daily light changes. Photic input is relayed to the suprachiasmatic nucleus to entrain the master clock, which matches behaviour to environmental changes. Circadian organization of the mouse retina involves coordinated, layer-specific oscillators, but so far little is known about the cone photoreceptor clock and its role in the circadian system. Using the cone-only Nrl-/- mouse model we show that cones contain a functional self-sustained molecular clockwork. By bioluminescence-combined imaging we also show that cones provide substantial input to the retinal clock network. Furthermore, we found that light entrainment and negative masking in cone-only mice are subtly altered and that constant light displayed profound effects on their central clock. Thus, our study demonstrates the contribution of cones to retinal circadian organisation and their role in finely tuning behaviour to environmental conditions.


Author(s):  
Ruifeng Cao

Circadian rhythm is the approximately 24-hour rhythmicity that regulates physiology and behavior in a variety of organisms. The mammalian circadian system is organized in a hierarchical manner. Molecular circadian oscillations driven by genetic feedback loops are found in individual cells, whereas circadian rhythms in different systems of the body are orchestrated by the master clock in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. SCN receives photic input from retina and synchronizes endogenous rhythms with the external light/dark cycles. SCN regulates circadian rhythms in the peripheral oscillators via neural and humoral signals, which account for daily fluctuations of the physiological processes in these organs. Disruption of circadian rhythms can cause health problems and circadian dysfunction has been linked to many human diseases.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0249215
Author(s):  
Daniela Ruiz ◽  
Saffia T. Bajwa ◽  
Naisarg Vanani ◽  
Tanvir A. Bajwa ◽  
Daniel J. Cavanaugh

The circadian system produces ~24-hr oscillations in behavioral and physiological processes to ensure that they occur at optimal times of day and in the correct temporal order. At its core, the circadian system is composed of dedicated central clock neurons that keep time through a cell-autonomous molecular clock. To produce rhythmic behaviors, time-of-day information generated by clock neurons must be transmitted across output pathways to regulate the downstream neuronal populations that control the relevant behaviors. An understanding of the manner through which the circadian system enacts behavioral rhythms therefore requires the identification of the cells and molecules that make up the output pathways. To that end, we recently characterized theDrosophilapars intercerebralis (PI) as a major circadian output center that lies downstream of central clock neurons in a circuit controlling rest:activity rhythms. We have conducted single-cell RNA sequencing (scRNAseq) to identify potential circadian output genes expressed by PI cells, and used cell-specific RNA interference (RNAi) to knock down expression of ~40 of these candidate genes selectively within subsets of PI cells. We demonstrate that knockdown of theslowpoke(slo) potassium channel in PI cells reliably decreases circadian rest:activity rhythm strength. Interestingly,slomutants have previously been shown to have aberrant rest:activity rhythms, in part due to a necessary function ofslowithin central clock cells. However, rescue ofsloin all clock cells does not fully reestablish behavioral rhythms, indicating that expression in non-clock neurons is also necessary. Our results demonstrate thatsloexerts its effects in multiple components of the circadian circuit, including PI output cells in addition to clock neurons, and we hypothesize that it does so by contributing to the generation of daily neuronal activity rhythms that allow for the propagation of circadian information throughout output circuits.


2001 ◽  
Vol 38-40 ◽  
pp. 607-614 ◽  
Author(s):  
W.Otto Friesen ◽  
Gerta Fleissner ◽  
Günther Fleissner

Sign in / Sign up

Export Citation Format

Share Document