scholarly journals In vivo evaluation of the effect of lithium on peripheral circadian clocks by real-time monitoring of clock gene expression in near-freely moving mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yuka Sawai ◽  
Takezo Okamoto ◽  
Yugo Muranaka ◽  
Rino Nakamura ◽  
Ritsuko Matsumura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Real Time ◽  
Clock Gene ◽  
Circadian Clocks ◽  
Real Time Monitoring ◽  
In Vivo Evaluation ◽  
Clock Gene Expression ◽  
Freely Moving

scholarly journals In vivo imaging of clock gene expression in multiple tissues of freely moving mice

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Toshiyuki Hamada ◽  
Kenneth Sutherland ◽  
Masayori Ishikawa ◽  
Naoki Miyamoto ◽  
Sato Honma ◽  
...  
Keyword(s):  
Gene Expression ◽  
In Vivo Imaging ◽  
Clock Gene ◽  
Clock Gene Expression ◽  
Freely Moving

scholarly journals Reciprocal Regulation of Brain and Muscle Arnt-Like Protein 1 and Peroxisome Proliferator-Activated Receptor α Defines a Novel Positive Feedback Loop in the Rodent Liver Circadian Clock

2006 ◽  
Vol 20 (8) ◽  
pp. 1715-1727 ◽  
Author(s):  
Laurence Canaple ◽  
Juliette Rambaud ◽  
Ouria Dkhissi-Benyahya ◽  
Béatrice Rayet ◽  
Nguan Soon Tan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Circadian Rhythm ◽  
Feedback Loop ◽  
Clock Gene ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Reciprocal Regulation ◽  
Clock Gene Expression ◽  
Regulatory Feedback Loop

Abstract Recent evidence has emerged that peroxisome proliferator-activated receptor α (PPARα), which is largely involved in lipid metabolism, can play an important role in connecting circadian biology and metabolism. In the present study, we investigated the mechanisms by which PPARα influences the pacemakers acting in the central clock located in the suprachiasmatic nucleus and in the peripheral oscillator of the liver. We demonstrate that PPARα plays a specific role in the peripheral circadian control because it is required to maintain the circadian rhythm of the master clock gene brain and muscle Arnt-like protein 1 (bmal1) in vivo. This regulation occurs via a direct binding of PPARα on a potential PPARα response element located in the bmal1 promoter. Reversely, BMAL1 is an upstream regulator of PPARα gene expression. We further demonstrate that fenofibrate induces circadian rhythm of clock gene expression in cell culture and up-regulates hepatic bmal1 in vivo. Together, these results provide evidence for an additional regulatory feedback loop involving BMAL1 and PPARα in peripheral clocks.

scholarly journals In vivo endotoxin synchronizes and suppresses clock gene expression in human peripheral blood leukocytes*

2010 ◽  
Vol 38 (3) ◽  
pp. 751-758 ◽  
Author(s):  
Beatrice Haimovich ◽  
Jacqueline Calvano ◽  
Adrian D. Haimovich ◽  
Steve E. Calvano ◽  
Susette M. Coyle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Peripheral Blood ◽  
Clock Gene ◽  
Human Peripheral Blood ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Clock Gene Expression

scholarly journals Real time, in vivo measurement of neuronal and peripheral clocks in Drosophila melanogaster

2022 ◽  
Author(s):  
Peter S Johnstone ◽  
Maite Ogueta ◽  
Inan Top ◽  
Sheyum Syed ◽  
Ralf Stanewsky ◽  
...  
Keyword(s):  
Gene Expression ◽  
Real Time ◽  
Circadian Clocks ◽  
Specific Gene ◽  
Tissue Specific ◽  
In Vivo Measurement ◽  
Neuronal Tissues ◽  
Peripheral Clocks ◽  
The Brain

Circadian clocks are highly conserved transcriptional regulators that control 24-hour oscillations in gene expression, physiological function, and behavior. Circadian clocks exist in almost every tissue and are thought to control tissue-specific gene expression and function, synchronized by the brain clock. Many disease states are associated with loss of circadian regulation. How and when circadian clocks fail during pathogenesis remains largely unknown because it is currently difficult to monitor tissue-specific clock function in intact organisms. Here, we developed a method to directly measure the transcriptional oscillation of distinct neuronal and peripheral clocks in live, intact Drosophila, which we term Locally Activatable BioLuminescence or LABL. Using this method, we observed that specific neuronal and peripheral clocks exhibit distinct transcription properties. Loss of the receptor for PDF, a circadian neurotransmitter critical for the function of the brain clock, disrupts circadian locomotor activity but not all tissue-specific circadian clocks; we found that, while peripheral clocks in non-neuronal tissues were less stable after the loss of PDF signaling, they continued to oscillate. This result suggests that the presumed dominance of the brain clock in regulating peripheral clocks needs to be re-examined. This result further demonstrates that LABL allows rapid, affordable, and direct real-time monitoring of clocks in vivo.

scholarly journals The Circadian Oscillator of the Cerebellum: Triiodothyronine Regulates Clock Gene Expression in Granule Cells in vitro and in the Cerebellum of Neonatal Rats in vivo

2021 ◽  
Vol 12 ◽  
Author(s):  
Tenna Bering ◽  
Henrik Hertz ◽  
Martin Fredensborg Rath
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Granule Cells ◽  
Clock Genes ◽  
Circadian Oscillator ◽  
Neonatal Rats ◽  
Clock Gene Expression ◽  
Mixed Gender

The central circadian clock resides in the suprachiasmatic nucleus (SCN) of the hypothalamus, but an SCN-dependent molecular circadian oscillator is present in the cerebellar cortex. Recent findings suggest that circadian release of corticosterone is capable of driving the circadian oscillator of the rat cerebellum. To determine if additional neuroendocrine signals act to shape cerebellar clock gene expression, we here tested the role of the thyroid hormone triiodothyronine (T3) in regulation of the cerebellar circadian oscillator. In cultured cerebellar granule cells from mixed-gender neonatal rats, T3 treatment affected transcript levels of the clock genes Per2, Arntl, Nr1d1, and Dbp, suggesting that T3 acts directly on granule cells to control the circadian oscillator. We then used two different in vivo protocols to test the role of T3 in adult female rats: Firstly, a single injection of T3 did not influence clock gene expression in the cerebellum. Secondly, we established a surgical rat model combining SCN lesion with a programmable micropump infusing circadian physiological levels of T3; however, rhythmic infusion of T3 did not reestablish differential clock gene expression between day and night in SCN lesioned rats. To test if the effects of T3 observed in vitro were related to the developmental stage, acute injections of T3 were performed in mixed-gender neonatal rats in vivo; this procedure significantly affected cerebellar expression of the clock genes Per1, Per2, Nr1d1, and Dbp. Developmental comparisons showed rhythmic expression of all clock genes analyzed in the cerebellum of adult rats only, whereas T3 responsiveness was limited to neonatal animals. Thus, T3 shapes cerebellar clock gene profiles in early postnatal stages, but it does not represent a systemic circadian regulatory mechanism linking the SCN to the cerebellum throughout life.

scholarly journals Necdin regulates BMAL1 stability and circadian clock through SGT1-HSP90 chaperone machinery

2020 ◽  
Vol 48 (14) ◽  
pp. 7944-7957
Author(s):  
Renbin Lu ◽  
Yufan Dong ◽  
Jia-Da Li
Keyword(s):  
Gene Expression ◽  
Circadian Clock ◽  
Clock Gene ◽  
Ubiquitin Proteasome System ◽  
Circadian Clocks ◽  
Clock Gene Expression ◽  
Ubiquitin Proteasome ◽  
Hsp90 Chaperone ◽  
Abnormal Behaviors ◽  
Clock Protein

Abstract Circadian clocks are endogenous oscillators that control ∼24-hour physiology and behaviors in virtually all organisms. The circadian oscillator comprises interconnected transcriptional and translational feedback loops, but also requires finely coordinated protein homeostasis including protein degradation and maturation. However, the mechanisms underlying the mammalian clock protein maturation is largely unknown. In this study, we demonstrate that necdin, one of the Prader-Willi syndrome (PWS)-causative genes, is highly expressed in the suprachiasmatic nuclei (SCN), the pacemaker of circadian clocks in mammals. Mice deficient in necdin show abnormal behaviors during an 8-hour advance jet-lag paradigm and disrupted clock gene expression in the liver. By using yeast two hybrid screening, we identified BMAL1, the core component of the circadian clock, and co-chaperone SGT1 as two necdin-interactive proteins. BMAL1 and SGT1 associated with the N-terminal and C-terminal fragments of necdin, respectively. Mechanistically, necdin enables SGT1-HSP90 chaperone machinery to stabilize BMAL1. Depletion of necdin or SGT1/HSP90 leads to degradation of BMAL1 through the ubiquitin–proteasome system, resulting in alterations in both clock gene expression and circadian rhythms. Taken together, our data identify the PWS-associated protein necdin as a novel regulator of the circadian clock, and further emphasize the critical roles of chaperone machinery in circadian clock regulation.

Sign in / Sign up

Export Citation Format

Share Document