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The Circadian Clock, Reward, and Memory  [PDF]
Urs Albrecht
Frontiers in Molecular Neuroscience , 2011, DOI: 10.3389/fnmol.2011.00041
Abstract: During our daily activities, we experience variations in our cognitive performance, which is often accompanied by cravings for small rewards, such as consuming coffee or chocolate. This indicates that the time of day, cognitive performance, and reward may be related to one another. This review will summarize data that describe the influence of the circadian clock on addiction and mood-related behavior and put the data into perspective in relation to memory processes.
Traumatic Brain Injury-Induced Dysregulation of the Circadian Clock  [PDF]
Deborah R. Boone, Stacy L. Sell, Maria-Adelaide Micci, Jeanna M. Crookshanks, Margaret Parsley, Tatsuo Uchida, Donald S. Prough, Douglas S. DeWitt, Helen L. Hellmich
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046204
Abstract: Circadian rhythm disturbances are frequently reported in patients recovering from traumatic brain injury (TBI). Since circadian clock output is mediated by some of the same molecular signaling cascades that regulate memory formation (cAMP/MAPK/CREB), cognitive problems reported by TBI survivors may be related to injury-induced dysregulation of the circadian clock. In laboratory animals, aberrant circadian rhythms in the hippocampus have been linked to cognitive and memory dysfunction. Here, we addressed the hypothesis that circadian rhythm disruption after TBI is mediated by changes in expression of clock genes in the suprachiasmatic nuclei (SCN) and hippocampus. After fluid-percussion TBI or sham surgery, male Sprague-Dawley rats were euthanized at 4 h intervals, over a 48 h period for tissue collection. Expression of circadian clock genes was measured using quantitative real-time PCR in the SCN and hippocampus obtained by laser capture and manual microdissection respectively. Immunofluorescence and Western blot analysis were used to correlate TBI-induced changes in circadian gene expression with changes in protein expression. In separate groups of rats, locomotor activity was monitored for 48 h. TBI altered circadian gene expression patterns in both the SCN and the hippocampus. Dysregulated expression of key circadian clock genes, such as Bmal1 and Cry1, was detected, suggesting perturbation of transcriptional-translational feedback loops that are central to circadian timing. In fact, disruption of circadian locomotor activity rhythms in injured animals occurred concurrently. These results provide an explanation for how TBI causes disruption of circadian rhythms as well as a rationale for the consideration of drugs with chronobiotic properties as part of a treatment strategy for TBI.
Circadian rhythms and memory formation: regulation by chromatin remodeling  [PDF]
Saurabh Sahar,Paolo Sassone-Corsi
Frontiers in Molecular Neuroscience , 2012, DOI: 10.3389/fnmol.2012.00037
Abstract: Epigenetic changes, such as DNA methylation or histone modification, can remodel the chromatin and regulate gene expression. Remodeling of chromatin provides an efficient mechanism of transducing signals, such as light or nutrient availability, to regulate gene expression. CLOCK:BMAL1 mediated activation of clock-controlled genes (CCGs) is coupled to circadian changes in histone modification at their promoters. Several chromatin modifiers, such as the deacetylases SIRT1 and HDAC3 or methyltransferase MLL1, have been shown to be recruited to the promoters of the CCGs in a circadian manner. Interestingly, the central element of the core clock machinery, the transcription factor CLOCK, also possesses histone acetyltransferase activity. Rhythmic expression of the CCGs is abolished in the absence of these chromatin modifiers. Recent research has demonstrated that chromatin remodeling is at the cross-roads of circadian rhythms and regulation of metabolism and aging. It would be of interest to identify if similar pathways exist in the epigenetic regulation of memory formation.
Circadian clocks and memory: time-place learning  [PDF]
C. K. Mulder,M. P. Gerkema,E. A. Van der Zee
Frontiers in Molecular Neuroscience , 2013, DOI: 10.3389/fnmol.2013.00008
Abstract: Time-Place learning (TPL) refers to the ability of animals to remember important events that vary in both time and place. This ability is thought to be functional to optimize resource localization and predator avoidance in a circadian changing environment. Various studies have indicated that animals use their circadian system for TPL. However, not much is known about this specific role of the circadian system in cognition. This review aims to put TPL in a broader context and to provide an overview of historical background, functional aspects, and future perspectives of TPL. Recent advances have increased our knowledge on establishing TPL in a laboratory setting, leading to the development of a behavioral paradigm demonstrating the circadian nature of TPL in mice. This has enabled the investigation of circadian clock components on a functional behavioral level. Circadian TPL (cTPL) was found to be Cry clock gene dependent, confirming the essential role of Cry genes in circadian rhythms. In contrast, preliminary results have shown that cTPL is independent of Per genes. Circadian system decline with aging predicts that cTPL is age sensitive, potentially qualifying TPL as a functional model for episodic memory and aging. The underlying neurobiological mechanism of TPL awaits further examination. Here we discuss some putative mechanisms.
The Circadian Clock Coordinates Ribosome Biogenesis  [PDF]
Céline Jouffe equal contributor,Gaspard Cretenet equal contributor,Laura Symul,Eva Martin,Florian Atger,Felix Naef,Frédéric Gachon
PLOS Biology , 2013, DOI: 10.1371/journal.pbio.1001455
Abstract: Biological rhythms play a fundamental role in the physiology and behavior of most living organisms. Rhythmic circadian expression of clock-controlled genes is orchestrated by a molecular clock that relies on interconnected negative feedback loops of transcription regulators. Here we show that the circadian clock exerts its function also through the regulation of mRNA translation. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in ribosome biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation. Moreover, the circadian oscillator directly regulates the transcription of ribosomal protein mRNAs and ribosomal RNAs. Thus the circadian clock exerts a major role in coordinating transcription and translation steps underlying ribosome biogenesis.
Circadian clock, cell cycle and cancer
Cansu ?zbayer,?rfan De?irmenci
Dicle Medical Journal , 2011,
Abstract: There are a few rhythms of our daily lives that we are under the influence. One of them is characterized by predictable changes over a 24-hour timescale called circadian clock. This cellular clock is coordinated by the suprachiasmatic nucleus in the anterior hypothalamus. The clock consist of an autoregulatory transcription-translation feedback loop compose of four genes/proteins; BMAL1, Clock, Cyrptochrome, and Period. BMAL 1 and Clock are transcriptional factors and Period and Cyrptochrome are their targets. Period and Cyrptochrome dimerize in the cytoplasm to enter the nucleus where they inhibit Clock/BMAL activity.It has been demonstrate that circadian clock plays an important role cellular proliferation, DNA damage and repair mechanisms, checkpoints, apoptosis and cancer.
Network Features of the Mammalian Circadian Clock  [PDF]
Julie E. Baggs,Tom S. Price,Luciano DiTacchio,Satchidananda Panda,Garret A. FitzGerald,John B. Hogenesch
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000052
Abstract: The mammalian circadian clock is a cell-autonomous system that drives oscillations in behavior and physiology in anticipation of daily environmental change. To assess the robustness of a human molecular clock, we systematically depleted known clock components and observed that circadian oscillations are maintained over a wide range of disruptions. We developed a novel strategy termed Gene Dosage Network Analysis (GDNA) in which small interfering RNA (siRNA)-induced dose-dependent changes in gene expression were used to build gene association networks consistent with known biochemical constraints. The use of multiple doses powered the analysis to uncover several novel network features of the circadian clock, including proportional responses and signal propagation through interacting genetic modules. We also observed several examples where a gene is up-regulated following knockdown of its paralog, suggesting the clock network utilizes active compensatory mechanisms rather than simple redundancy to confer robustness and maintain function. We propose that these network features act in concert as a genetic buffering system to maintain clock function in the face of genetic and environmental perturbation.
Network Features of the Mammalian Circadian Clock  [PDF]
Julie E Baggs,Tom S Price,Luciano DiTacchio,Satchidananda Panda,Garret A FitzGerald,John B Hogenesch
PLOS Biology , 2009, DOI: 10.1371/journal.pbio.1000052
Abstract: The mammalian circadian clock is a cell-autonomous system that drives oscillations in behavior and physiology in anticipation of daily environmental change. To assess the robustness of a human molecular clock, we systematically depleted known clock components and observed that circadian oscillations are maintained over a wide range of disruptions. We developed a novel strategy termed Gene Dosage Network Analysis (GDNA) in which small interfering RNA (siRNA)-induced dose-dependent changes in gene expression were used to build gene association networks consistent with known biochemical constraints. The use of multiple doses powered the analysis to uncover several novel network features of the circadian clock, including proportional responses and signal propagation through interacting genetic modules. We also observed several examples where a gene is up-regulated following knockdown of its paralog, suggesting the clock network utilizes active compensatory mechanisms rather than simple redundancy to confer robustness and maintain function. We propose that these network features act in concert as a genetic buffering system to maintain clock function in the face of genetic and environmental perturbation.
A circadian clock in the cardiovascular system  [cached]
Simon Frantz
Genome Biology , 2001, DOI: 10.1186/gb-spotlight-20010710-02
Abstract: All eukaryotes display changes in biochemical or physiological behaviour that are governed by the day/night cycle; for example, melatonin levels rise during the night and falling during the day. The 'master clock' in humans is situated in the suprachiasmatic nucleus (SCN), an area of the brain that consists of a cluster of around 10,000 neurons synchronized to fire rhythmically and generate a coordinated circadian rhythmic output.One of the most intensive areas of biological research has involved discovering the factors that drive these circadian rhythms. Studies have found interacting positive and negative transcriptional-translational feedback loops are important. The best-characterized feedback loop in the mouse involves the regulation of three Period genes (mPER1-mPer3) and two Cryptochrome genes (mCRY1 and mCRY2).Transcription of mPer and mCry genes is thought to be driven by accumulating heterodimers of the CLOCK and BMAL(MOP3) proteins; the heterodimers activate the genes by binding to consensus E-box elements. Subsequently, complexes of mPER and mCRY proteins enter the nucleus, where they shut off CLOCK-BMAL1-mediated transcription. At the same time, mPER2 upregulates levels of Bmal1 RNA (by a currently unknown mechanism), leading to the formation of CLOCK:BMAL1 heterodimers which drive mPer/mCry transcription and restart the cycle.Recently, molecular clocks have also been uncovered in peripheral tissues, such as the liver, kidney and heart. Circadian rhythms in mPer RNA abundance had been observed, although their phase of oscillation is delayed three to nine hours relative to the oscillation in the SCN. Studies on both isolated cells and SCN-deficient animals suggested that these peripheral oscillations might be driven or synchronized by the SCN, while other findings indicated that humoral signals could be involved, although the mechanism was poorly understood.This led researchers to investigate blood pressure, because it exhibits a circadian variability th
Epigenetic Control of Circadian Clock Operation during Development  [PDF]
Chengwei Li,Changxia Gong,Shuang Yu,Jianguo Wu,Xiaodong Li
Genetics Research International , 2012, DOI: 10.1155/2012/845429
Abstract: The molecular players of circadian clock oscillation have been identified and extensively characterized. The epigenetic mechanisms behind the circadian gene expression control has also been recently studied, although there are still details to be illucidated. In this review, we briefly summarize the current understanding of the mammalian clock. We also provide evidence for the lack of circadian oscillation in particular cell types. As the circadian clock has intimate interaction with the various cellular functions in different type of cells, it must have plasticity and specicity in its operation within different epigenetic environments. The lack of circadian oscillation in certain cells provide an unique opportunity to study the required epigenetic environment in the cell that permit circadian oscillation and to idenfify key influencing factors for proper clock function. How epigenetic mechansims, including DNA methylaiton and chromatin modifications, participate in control of clock oscillation still awaits future studies at the genomic scale. 1. Introduction Mammals have overt circadian rhythms in their physiology and behavior, orchestrated by the suprachiasmatic nucleus of the anterior hypothalamus [1, 2]. The endogenous circadian clock enables organisms to anticipate the regular daily changes in the environment and temporally organize their life activities [3, 4]. Fundamentally, circadian timing functions exist at the cellular level not only for suprachiasmatic neurons, but also for cells of various peripheral tissues [5–9]. 2. A Brief Overview of Clockwork Mechanisms The past two decades witnessed the rapid pace in gaining in-depth understanding of mammalian clockwork operation. Circadian oscillations are generated at the molecular level by a set of clock genes [10–12]. The mapping and cloning of the ClockΔ19 mutation through ENU mutagenesis and positional cloning set the stage for elucidation of mammalian clockwork mechanisms [13–15]. BMAL1 was soon identified to be the dimerization partner of CLOCK to drive clock gene expression [16, 17]. Mouse Per genes were also identified and found to be driven by the CLOCK/BMAL1 dimer [18–20]. CRY1 and CRY2 were later found to have essential roles in the integrity of the circadian clock through inhibiting CLOCK/BMAL1-mediated transcription activation [21, 22]. Thus CLOCK and BMAL1 form the positive limb, while CRY and PER proteins form the negative limb of the transcriptional feedback loop [23]. Later on, more details were elucidated and revisions were made for the clockwork model, including the antagonistic
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