scholarly journals Suprachiasmatic Regulation of Circadian Rhythms of Gene Expression in Hamster Peripheral Organs: Effects of Transplanting the Pacemaker

2006 ◽  
Vol 26 (24) ◽  
pp. 6406-6412 ◽  
Author(s):  
H. Guo ◽  
J. M. Brewer ◽  
M. N. Lehman ◽  
E. L. Bittman
2006 ◽  
Vol 27 (1) ◽  
pp. 18-19
Author(s):  
Eric L. Bittman ◽  
Anastasia Nikiforov ◽  
Ruth Harris ◽  
Judy McKinley Brewer

2020 ◽  
Vol 3 (1) ◽  
pp. 58-76 ◽  
Author(s):  
Bohan Rong ◽  
Qiong Wu ◽  
Chao Sun

Melatonin is a well-known molecule for its involvement in circadian rhythm regulation and its contribution to protection against oxidative stress in organisms including unicellular alga, animals and plants. Currently, the bio-regulatory effects of melatonin on the physiology of various peripheral tissues have drawn a great attention of scientists. Although melatonin was previously defined as a neurohormone secreted from pineal gland, recently it has been identified that virtually, every cell has the capacity to synthesize melatonin and the locally generated melatonin has multiple pathophysiological functions, including regulations of obesity and metabolic syndromes. Herein, we focus on the effects of melatonin on fat deposition in various peripheral organs/tissues. The two important regulatory mechanisms related to the topic, i.e., the improvements of circadian rhythms and antioxidative capacity will be thoroughly discussed since they are linked to several biomarkers involved in obesity and energy imbalance, including metabolism and immunity. Furthermore, several other functions of melatonin which may serve to prevent or promote obesity and energy dysmetabolism-induced pathological states are also addressed. The organs of special interest include liver, pancreas, skeletal muscle, adipose tissue and the gut microbiota.


1998 ◽  
Vol 292 (2) ◽  
pp. 345-354 ◽  
Author(s):  
Xiao-Cun Wang ◽  
Kenneth I. Strauss ◽  
Quy N. Ha ◽  
Satish Nagula ◽  
Matthew E. Wolpoe ◽  
...  

Neuron ◽  
1991 ◽  
Vol 6 (5) ◽  
pp. 753-766 ◽  
Author(s):  
Xin Liu ◽  
Qiang Yu ◽  
Zuoshi Huang ◽  
Laurence J. Zwiebel ◽  
Jeffrey C. Hall ◽  
...  

2019 ◽  
Vol 34 (2) ◽  
pp. 144-153 ◽  
Author(s):  
Andrew D. Beale ◽  
Emily Kruchek ◽  
Stephen J. Kitcatt ◽  
Erin A. Henslee ◽  
Jack S.W. Parry ◽  
...  

Temperature compensation and period determination by casein kinase 1 (CK1) are conserved features of eukaryotic circadian rhythms, whereas the clock gene transcription factors that facilitate daily gene expression rhythms differ between phylogenetic kingdoms. Human red blood cells (RBCs) exhibit temperature-compensated circadian rhythms, which, because RBCs lack nuclei, must occur in the absence of a circadian transcription-translation feedback loop. We tested whether period determination and temperature compensation are dependent on CKs in RBCs. As with nucleated cell types, broad-spectrum kinase inhibition with staurosporine lengthened the period of the RBC clock at 37°C, with more specific inhibition of CK1 and CK2 also eliciting robust changes in circadian period. Strikingly, inhibition of CK1 abolished temperature compensation and increased the Q10 for the period of oscillation in RBCs, similar to observations in nucleated cells. This indicates that CK1 activity is essential for circadian rhythms irrespective of the presence or absence of clock gene expression cycles.


PLoS ONE ◽  
2009 ◽  
Vol 4 (5) ◽  
pp. e5650 ◽  
Author(s):  
Cathy Cailotto ◽  
Jun Lei ◽  
Jan van der Vliet ◽  
Caroline van Heijningen ◽  
Corbert G. van Eden ◽  
...  

2001 ◽  
Vol 280 (4) ◽  
pp. R1206-R1212 ◽  
Author(s):  
Jean-Christophe Leloup ◽  
Albert Goldbeter

With the use of a molecular model for circadian rhythms in Drosophila based on transcriptional regulation, we show how a single, critical pulse of light can permanently suppress circadian rhythmicity, whereas a second light pulse can restore the abolished rhythm. The phenomena occur via the pulsatile induction of either protein degradation or gene expression in conditions in which a stable steady state coexists with stable circadian oscillations of the limit cycle type. The model indicates that suppression by a light pulse can only be accounted for by assuming that the biochemical effects of such a pulse much outlast its actual duration. We determine the characteristics of critical pulses suppressing the oscillations as a function of the phase at which the rhythm is perturbed. The model predicts how the amplitude and duration of the biochemical changes induced by critical pulses vary with this phase. The results provide a molecular, dynamic explanation for the long-term suppression of circadian rhythms observed in a variety of organisms in response to a single light pulse and for the subsequent restoration of the rhythms by a second light pulse.


1992 ◽  
Vol 2 (1) ◽  
pp. 51
Author(s):  
Joseph S Takahashi

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