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Rhythmic Expression (rhythmic + expression)

Distribution by Scientific Domains

Life Sciences	88%

Selected Abstracts

Rhythmic expression of clock genes in the ependymal cell layer of the third ventricle of rodents is independent of melatonin signaling

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2008
Shinobu Yasuo
Abstract Reproductive physiology is regulated by the photoperiod in many mammals. Decoding of the photoperiod involves circadian clock mechanisms, although the molecular basis remains unclear. Recent studies have shown that the ependymal cell layer lining the infundibular recess of the third ventricle (EC) is a key structure for the photoperiodic gonadal response. The EC exhibits daylength-dependent changes in the expression of photoperiodic output genes, including the type 2 deiodinase gene (Dio2,). Here we investigated whether clock genes (Per1 and Bmal1) and the albumin D-binding protein gene (Dbp) are expressed in the EC of Syrian hamsters, and whether their expression differs under long-day and short-day conditions. Expression of all three genes followed a diurnal rhythm; expression of Per1 and Dbp in the EC peaked around lights-off, and expression of Bmal1 peaked in the early light phase. The amplitude of Per1 and Dbp expression was higher in hamsters kept under long-day conditions than in those kept under short-day conditions. Notably, the expression of these genes was not modified by exogenous melatonin within 25 h after injection, whereas Dio2 expression was inhibited 19 h after injection. Targeted melatonin receptor (MT1, MT2, and both MT1 and MT2) disruption in melatonin-proficient C3H mice did not affect the rhythmic expression of Per1 in the EC. These data show the existence of a molecular clock in the rodent EC. In the hamster, this clock responds to long-term changes in the photoperiod, but is independent of acute melatonin signals. In mice, the EC clock is not affected by deletion of melatonin receptors. [source]

A hVIPR transgene as a novel tool for the analysis of circadian function in the mouse suprachiasmatic nucleus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2003
V. M. King
Abstract A mouse bearing a novel transgene encoding the human VPAC2 receptor (hVIPR; Shen et al. (2000) PNAS, 97, 11575,11580) was used to investigate circadian function in the hypothalamic suprachiasmatic nuclei (SCN). Neurons expressing hVPAC2R, detected by a beta-galactosidase (,-GAL) tag, have a distinct distribution within the SCN, closely matching that of neurophysin (NP) neurons and extending into the region of peptide histidine isoleucine (PHI) cells. In common with NP and PHI cells, neurons expressing hVPAC2R are circadian in nature, as revealed by synchronous rhythmic expression of mPERIOD (mPER) proteins. A population of SCN cells not expressing PHI, NP or hVPAC2R exhibited circadian PER expression antiphasic with the rest of the SCN. Nocturnal light exposure induced mPER1 in the ventral SCN and mPER2 widely across the nucleus. Induction of nuclear mPER2 in hVPAC2R cells confirmed their photic responsiveness. Having established their circadian properties, we tested the utility of SCN neurons expressing the hVIPR transgene as functionally and anatomically explicit markers for SCN tissue grafts. Prenatal SCN tissue from hVIPR transgenic pups survived transplantation into adult CD1 mice, and expressed ,-GAL, PER and PHI. Over a series of studies, hVIPR transgenic SCN grafts restored circadian activity rhythms to 17 of 72 arrhythmic SCN lesioned recipients (23.6%). By using heterozygous hVIPR transgenic grafts on a heterozygous Clock mutant background we confirmed that restored activity rhythms were conferred by the donor tissue. We conclude that the hVIPR transgene is a powerful and flexible tool for examination of circadian function in the mouse SCN. [source]

Spatial and temporal variation of passer Per2 gene expression in two distinct cell groups of the suprachiasmatic hypothalamus in the house sparrow (Passer domesticus)

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2002
Ute Abraham
Abstract In mammals, the major pacemaker controlling circadian rhythmicity is located in the hypothalamic suprachiasmatic nuclei. Although there is evidence for the presence of a hypothalamic circadian oscillator in birds from lesioning studies, neuroanatomical, neurochemical and functional investigations have failed to identify its exact location. Two cell groups in the avian hypothalamus have been shown to bear characteristics of the mammalian suprachiasmatic nucleus: the suprachiasmatic nucleus and the lateral hypothalamic retinorecipient nucleus. We cloned an avian period homologue (pPer2) and investigated the temporal and spatial expression pattern of this gene in the house sparrow hypothalamus using in situ hybridization. Applying quantitative morphometry, we found rhythmic expression of pPer2 during light,dark as well as in constant conditions in the suprachiasmatic nucleus and in the lateral hypothalamus. The temporal and spatial distribution of pPer2 expression in the suprachiasmatic nucleus suggest a longitudinal compartmentalization of the nucleus with period gene expression being initiated in the most rostral portion of the suprachiasmatic nucleus before lights on. In the lateral hypothalamus, phasing of pPer2 -rhythmicity appeared different from the suprachiasmatic nucleus. The major difference between light,dark and constant conditions was a decrease in the amplitude of pPer2 rhythmicity in the suprachiasmatic nucleus. Our data demonstrate that, unlike in mammals, Per gene expression in the suprachiasmatic hypothalamus of the house sparrow is not confined to a single cell group, indicating a more complex organization of the circadian oscillator in the hypothalamus of birds. [source]

Clock-dependent and independent transcriptional control of the two isoforms from the mouse Ror,gene

GENES TO CELLS, Issue 12 2008
Valérie Mongrain
Accumulating evidence indicate that molecular mechanisms generating circadian rhythms display some degree of tissue-specificity. More specifically, distinct patterns of expression for nuclear receptors of the ROR family indicate that the transcriptional control of the clock gene Bmal1 differs among tissues. This study aims to investigate the expression of Ror,isoforms (Ror, and Ror,t) and characterize the molecular mechanisms underlying their tissue-specific expression. The expression of Ror, isoforms was assessed in mouse liver, muscle, thymus and testis throughout 24 h using quantitative RT-PCR. Although the expression of Ror, was rhythmic in the liver and thymus, it was constitutively expressed in muscle and testis. In contrast, the expression of Ror,t was constitutive in all four tissues. Furthermore, rhythmic expression of Ror, was impaired in Clock mutant mice whereas the mutation had no effect on Ror,t expression. In line with these findings, luciferase assays revealed that transcription of the Ror, promoter is clock-controlled whereas that of Ror,t promoter is essentially clock-independent. Our results provide insights into the molecular mechanisms that lead to differential expression of Ror, and Ror,t and are suggestive of a framework that might account for tissue-specific circadian regulation. [source]

Influence of Temperature on the Liver Circadian Clock in the Ruin Lizard Podarcis sicula

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 7 2007
Manuela Malatesta
Abstract Reptiles represent an interesting animal model to investigate the influence of temperature on molecular circadian clocks. The ruin lizard Podarcis sicula lives in a continental climate and it is subjected to wide range of environmental temperatures during the course of the year. As consequence, ruin lizard daily activity pattern includes either the hibernation or periods of inactivity determined by hypothermia. Here we showed the rhythmic expression of two clock genes, lPer2 and lClock, in the liver of active lizards exposed to summer photo-thermoperiodic conditions. Interestingly, the exposition of lizards to hypothermic conditions, typical of winter season, induced a strong dampening of clock genes mRNA rhythmicity with a coincident decrease of levels. We also examined the qualitative and quantitative distribution of lPER2 and lCLOCK protein in different cellular compartments during the 24-h cycle. In the liver of active lizards both proteins showed a rhythmic expression profile in all cellular compartments. After 3 days at 6°C, some temporal fluctuations of the lCLOCK and lPER2 are still detectable, although, with some marked modifications in respect to the values detected in the liver of active lizards. Besides demonstrating the influence of low temperature on the lizard liver circadian oscillators, present results could provide new essential information for comparative studies on the influence of temperature on the circadian system across vertebrate classes. Microsc. Res. Tech., 2007. © 2007 Wiley-Liss, Inc. [source]

The Neurospora circadian clock regulates a transcription factor that controls rhythmic expression of the output eas(ccg-2) gene

MOLECULAR MICROBIOLOGY, Issue 4 2001
Deborah Bell-Pedersen
The circadian clock provides a link between an organism's environment and its behaviour, temporally phasing the expression of genes in anticipation of daily environmental changes. Input pathways sense environmental information and interact with the clock to synchronize it to external cycles, and output pathways read out from the clock to impart temporal control on downstream targets. Very little is known about the regulation of outputs from the clock. In Neurospora crassa, the circadian clock transcriptionally regulates expression of the clock-controlled genes, including the well-characterized eas(ccg-2) gene. Dissection of the eas(ccg-2) gene promoter previously localized a 68 bp sequence containing an activating clock element (ACE) that is both necessary and sufficient for rhythmic activation of transcription by the circadian clock. Using electrophoretic mobility shift assays (EMSAs), we have identified light-regulated nuclear protein factors that bind specifically to the ACE in a time-of-day-dependent fashion, consistent with their role in circadian regulation of expression of eas(ccg-2). Nucleotides in the ACE that interact with the protein factors were determined using interference binding assays, and deletion of the core interacting sequences affected, but did not completely eliminate, rhythmic accumulation of eas(ccg-2) mRNA in vivo, whereas deletion of the entire ACE abolished the rhythm. These data indicate that redundant binding sites for the protein factors that promote eas(ccg-2) rhythms exist within the 68 bp ACE. The ACE binding complexes formed using protein extracts from cells with lesions in central components of the Neurospora circadian clock were identical to those formed with extracts from wild-type cells, indicating that other proteins directly control eas(ccg-2) rhythmic expression. These data suggest that the Neurospora crassa circadian clock regulates an unknown transcription factor, which in turn activates the expression of eas(ccg-2) at specific times of the day. [source]

RFI2, a RING-domain zinc finger protein, negatively regulates CONSTANS expression and photoperiodic flowering

THE PLANT JOURNAL, Issue 5 2006
Mingjie Chen
Summary The red and far-red light-absorbing phytochromes interact with the circadian clock, a central oscillator that sustains a 24-h period, to measure accurately seasonal changes in day-length and regulate the expression of several key flowering genes. The interactions and subsequent signalling steps upstream of the flowering genes such as CONSTANS (CO) and FLOWERING LOCUS T (FT) remain largely unknown. We report here that a photomorphogenic mutant, red and far-red insensitive 2-1 ( rfi2-1), flowered early particularly under long days. The rfi2-1 mutation also enhanced the expression of CO and FT under day/night cycles or constant light. Both co-2 and gigantea-2 (gi-2) were epistatic to rfi2-1 in their flowering responses. The gi-2 mutation was also epistatic to the rfi2-1 mutation in the expression of CO and hypocotyl elongation. However, the rfi2-1 mutation did not affect the expression of GI, a gene that mediates between the circadian clock and the expression of CO. Like many other flowering genes, the expression of RFI2 oscillated under day/night cycles and was rhythmic under constant light. The amplitude of the rhythmic expression of RFI2 was significantly reduced in phyB-9 or lhy-20 plants, and was also affected by the gi-2 mutation. As previously reported, the gi-2 mutation affects the period length and amplitude of CCA1 and LHY expression, and GI may act through a feedback loop to maintain a proper circadian function. We propose a regulatory step in which RFI2 represses the expression of CO, whereas GI may maintain the proper expression of RFI2 through its positive action on the circadian clock. The regulatory step serves to tune the circadian outputs that control the expression of CO and photoperiodic flowering. [source]