Circadian Transcription Factor NPAS2 and the NAD+‐Dependent Deacetylase SIRT1 Interact in the Mouse Nucleus Accumbens and Regulate Reward

Author(s):  
Darius D. Becker‐Krail ◽  
Puja K. Parekh ◽  
Kyle D. Ketchesin ◽  
Shintaro Yamaguchi ◽  
Jun Yoshino ◽  
...  
2001 ◽  
Vol 21 (4) ◽  
pp. 1207-1217 ◽  
Author(s):  
Michael J. McDonald ◽  
Michael Rosbash ◽  
Patrick Emery

ABSTRACT Transcriptional regulation plays an important role inDrosophila melanogaster circadian rhythms. The period promoter has been well studied, but the timeless promoter has not been analyzed in detail. Mutagenesis of the canonical E box in the timelesspromoter reduces but does not eliminate timeless mRNA cycling or locomotor activity rhythms. This is because there are at least two other cis-acting elements close to the canonical E box, which can also be transactivated by the circadian transcription factor dCLOCK. These E-box-like sequences cooperate with the canonical E-box element to promote high-amplitude transcription, which is necessary for wild-type rhythmicity.


Cell Reports ◽  
2020 ◽  
Vol 33 (7) ◽  
pp. 108394
Author(s):  
Suihong Huang ◽  
Ming Ho Choi ◽  
Hao Huang ◽  
Xin Wang ◽  
Yu Chen Chang ◽  
...  

2017 ◽  
Author(s):  
Anna M. Puszynska ◽  
Erin K. O’Shea

AbstractThe transcription factor RpaA is the master regulator of circadian transcription in cyanobacteria, driving genome-wide oscillations in mRNA abundance. Deletion ofrpaAhas no effect on viability in constant light conditions, but renders cells inviable in cycling conditions when light and dark periods alternate. We investigated the mechanisms underlying this viability defect, and demonstrate that therpaA-strain cannot maintain appropriate energy status at night, does not accumulate carbon reserves during the day, and is defective in transcription of genes crucial for utilization of carbohydrate stores at night. Reconstruction of carbon utilization pathways combined with provision of an external carbon source restores energy charge and viability of therpaA-strain in light/dark cycling conditions. Our observations highlight how a circadian program controls and temporally coordinates essential pathways in carbon metabolism to maximize fitness of cells facing periodic energy limitations.


2008 ◽  
Vol 22 (3) ◽  
pp. 331-345 ◽  
Author(s):  
H. Reinke ◽  
C. Saini ◽  
F. Fleury-Olela ◽  
C. Dibner ◽  
I. J. Benjamin ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Anna M Puszynska ◽  
Erin K O'Shea

The transcription factor RpaA is the master regulator of circadian transcription in cyanobacteria, driving genome-wide oscillations in mRNA abundance. Deletion of rpaA has no effect on viability in constant light conditions, but renders cells inviable in cycling conditions when light and dark periods alternate. We investigated the mechanisms underlying this viability defect, and demonstrate that the rpaA- strain cannot maintain appropriate energy status at night, does not accumulate carbon reserves during the day, and is defective in transcription of genes crucial for utilization of carbohydrate stores at night. Reconstruction of carbon utilization pathways combined with provision of an external carbon source restores energy charge and viability of the rpaA- strain in light/dark cycling conditions. Our observations highlight how a circadian output pathway controls and temporally coordinates essential pathways in carbon metabolism to maximize fitness of cells facing periodic energy limitations.


2020 ◽  
Author(s):  
S.H. Wood ◽  
M.M. Hindle ◽  
Y. Mizoro ◽  
Y. Cheng ◽  
B.R.C. Saer ◽  
...  

AbstractThe annual photoperiod cycle provides the critical environmental cue synchronizing rhythms of life in seasonal habitats. In 1936, Bünning proposed a circadian-based coincidence timer for photoperiodic synchronization in plants. Formal studies support the universality of this so-called coincidence timer, but we lack understanding of the mechanisms involved. Here we show in mammals that long photoperiods induce the circadian transcription factor BMAL2, in the pars tuberalis of the pituitary, and triggers summer biology through the eyes absent / thyrotrophin (EYA3 / TSH) pathway. Conversely, long-duration melatonin signals on short photoperiods induce circadian repressors including DEC1, suppressing BMAL2 and the EYA3/TSH pathway, triggering winter biology. These actions are associated with progressive genome-wide changes in chromatin state, elaborating the effect of the circadian coincidence timer. Hence, circadian clock-pituitary epigenetic pathway interactions form the basis of the mammalian coincidence timer mechanism. Our results constitute a blueprint for circadian-based seasonal timekeeping in vertebrates.


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