scholarly journals The synchronization and adaptation of Neurospora crassa circadian and conidiation rhythms to short light-dark cycles

2018 ◽  
Author(s):  
Huan Ma ◽  
Luyao Li ◽  
Jie Yan ◽  
Yin Zhang ◽  
Weirui Shi ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa ◽  
Metabolic Pathways ◽  
Diurnal Rhythms ◽  
Daily Rhythms ◽  
The Core ◽  
Ubiquitin E3 Ligase ◽  
Modeling And Experiments ◽  
High Intensity Light ◽  
Clock Protein

ABSTRACTCircadian clocks control the physiological and behavioral daily rhythms to adapt to the changing environment with a period of ~24 h. However, the influence and mechanism of extreme light-dark cycles on the circadian clock remain unclear. We show that, in the fungus Neurospora crassa under short LD cycles, both the growth rate and the ratio of microconidia production contributes to adaptation in LD12:12 (light for 12 h and dark for 12 h, periodically). Mathematical modeling and experiments demonstrate that in short LD cycles, the expression of the core clock protein FREQUENCY is entrained to the LD cycles when LD>3:3 while it free runs when T≤ LD3:3. We investigated the changes in circadian/diurnal rhythms under a series of different LD conditions, and the results showed that conidial rhythmicity can be adapted to the short LD cycles. We further demonstrate that the existence of unknown blue light photoreceptor(s) and the circadian clock might promote the conidiation rhythms that resonate with the environment. A high-intensity light induced the expression of a set of downstream genes involved in various metabolic pathways. The ubiquitin E3 ligase FWD-1 and the previously described CRY-dependent oscillator system were implicated in regulating conidiation under short LD conditions.

scholarly journals The Resonance and Adaptation of Neurospora crassa Circadian and Conidiation Rhyth ms to Short Light-Dark Cycles

2021 ◽  
Vol 8 (1) ◽  
pp. 27
Author(s):  
Huan Ma ◽  
Luyao Li ◽  
Jie Yan ◽  
Yin Zhang ◽  
Xiaohong Ma ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa ◽  
Circadian Clocks ◽  
Extreme Conditions ◽  
Behavioral Rhythms ◽  
The Core ◽  
Regulatory Aspects ◽  
Ubiquitin E3 Ligase ◽  
Modeling And Experiments ◽  
Clock Protein

Circadian clocks control the physiological and behavioral rhythms to adapt to the environment with a period of ~24 h. However, the influences and mechanisms of the extreme light/dark cycles on the circadian clock remain unclear. We showed that, in Neurospora crassa, both the growth and the microconidia production contribute to adaptation in LD12:12 (12 h light/12 h dark, periodically). Mathematical modeling and experiments demonstrate that in short LD cycles, the expression of the core clock protein FREQUENCY was entrained to the LD cycles when LD > 3:3 while it free ran when T ≤ LD3:3. The conidial rhythmicity can resonate with a series of different LD conditions. Moreover, we demonstrate that the existence of unknown blue light photoreceptor(s) and the circadian clock might promote the conidiation rhythms that resonate with the environment. The ubiquitin E3 ligase FWD-1 and the previously described CRY-dependent oscillator system were implicated in regulating conidiation under short LD conditions. These findings shed new light on the resonance of Neurospora circadian clock and conidiation rhythms to short LD cycles, which may benefit the understandings of both the basic regulatory aspects of circadian clock and the adaptation of physiological rhythms to the extreme conditions.

scholarly journals Intrinsic disorder is an essential characteristic of components in the conserved circadian circuit

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Jacqueline F. Pelham ◽  
Jay C. Dunlap ◽  
Jennifer M. Hurley
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa ◽  
Mus Musculus ◽  
Intrinsically Disordered Proteins ◽  
Intrinsic Disorder ◽  
Cellular Systems ◽  
Disordered Proteins ◽  
Circadian Timing ◽  
Intrinsically Disordered ◽  
The Core

Abstract Introduction The circadian circuit, a roughly 24 h molecular feedback loop, or clock, is conserved from bacteria to animals and allows for enhanced organismal survival by facilitating the anticipation of the day/night cycle. With circadian regulation reportedly impacting as high as 80% of protein coding genes in higher eukaryotes, the protein-based circadian clock broadly regulates physiology and behavior. Due to the extensive interconnection between the clock and other cellular systems, chronic disruption of these molecular rhythms leads to a decrease in organismal fitness as well as an increase of disease rates in humans. Importantly, recent research has demonstrated that proteins comprising the circadian clock network display a significant amount of intrinsic disorder. Main body In this work, we focus on the extent of intrinsic disorder in the circadian clock and its potential mechanistic role in circadian timing. We highlight the conservation of disorder by quantifying the extent of computationally-predicted protein disorder in the core clock of the key eukaryotic circadian model organisms Drosophila melanogaster, Neurospora crassa, and Mus musculus. We further examine previously published work, as well as feature novel experimental evidence, demonstrating that the core negative arm circadian period drivers FREQUENCY (Neurospora crassa) and PERIOD-2 (PER2) (Mus musculus), possess biochemical characteristics of intrinsically disordered proteins. Finally, we discuss the potential contributions of the inherent biophysical principals of intrinsically disordered proteins that may explain the vital mechanistic roles they play in the clock to drive their broad evolutionary conservation in circadian timekeeping. Conclusion The pervasive conservation of disorder amongst the clock in the crown eukaryotes suggests that disorder is essential for optimal circadian timing from fungi to animals, providing vital homeostatic cellular maintenance and coordinating organismal physiology across phylogenetic kingdoms. Graphical abstract

scholarly journals Transcriptional regulatory logic of the diurnal cycle in the mouse liver

2016 ◽  
Author(s):  
Jonathan Aryeh Sobel ◽  
Irina Krier ◽  
Teemu Andersin ◽  
Sunil Raghav ◽  
Donatella Canella ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Rna Polymerase Ii ◽  
Diurnal Cycle ◽  
Mouse Liver ◽  
Regulatory Elements ◽  
Dnase I ◽  
Diurnal Rhythms ◽  
Dynamic Binding ◽  
Pol Ii ◽  
The Core

AbstractMany organisms exhibit temporal rhythms in gene expression that propel diurnal cycles in physiology. In the liver of mammals, these rhythms are controlled by transcription-translation feedback loops of the core circadian clock and by feeding-fasting cycles. To better understand the regulatory interplay between the circadian clock and feeding rhythms, we mapped DNase I hypersensitive sites (DHSs) in mouse liver during a diurnal cycle. The intensity of DNase I cleavages cycled at a substantial fraction of all DHSs, suggesting that DHSs harbor regulatory elements that control rhythmic transcription. Using ChIP-seq, we found that hypersensitivity cycled in phase with RNA polymerase II (Pol II) loading and H3K27ac histone marks. We then combined the DHSs with temporal Pol II profiles in wild-type (WT) and Bmal1-/- livers to computationally identify transcription factors through which the core clock and feeding-fasting cycles control diurnal rhythms in transcription. While a similar number of mRNAs accumulated rhythmically in Bmal1-/- compared to WT livers, the amplitudes in Bmal1-/- were generally lower. The residual rhythms in Bmal1-/- reflected transcriptional regulators mediating feeding-fasting responses as well as responses to rhythmic systemic signals. Finally, the analysis of DNase I cuts at nucleotide resolution showed dynamically changing footprint consistent with dynamic binding of CLOCK:BMAL1 complexes. Structural modeling suggested that these footprints are driven by a transient hetero-tetramer binding configuration at peak activity. Together, our temporal DNase I mappings allowed us to decipher the global regulation of diurnal transcription rhythms in mouse liver.

scholarly journals Visualizing and Quantifying Intracellular Behavior and Abundance of the Core Circadian Clock Protein PERIOD2

2016 ◽  
Vol 26 (14) ◽  
pp. 1880-1886 ◽  
Author(s):  
Nicola J. Smyllie ◽  
Violetta Pilorz ◽  
James Boyd ◽  
Qing-Jun Meng ◽  
Ben Saer ◽  
...  
Keyword(s):  
Circadian Clock ◽  
The Core ◽  
Clock Protein

scholarly journals Cell-autonomous regulation of astrocyte activation by the circadian clock protein BMAL1

2018 ◽  
Author(s):  
Brian V. Lananna ◽  
Collin J. Nadarajah ◽  
Mariko Izumo ◽  
Michelle R. Cedeño ◽  
David D. Xiong ◽  
...  
Keyword(s):  
Circadian Clock ◽  
List Type ◽  
Brain Health ◽  
Glutathione S Transferase ◽  
Astrocyte Activation ◽  
The Core ◽  
A Cell ◽  
Clock Protein

SummaryCircadian clock dysfunction is a common symptom of aging and neurodegenerative diseases, though its impact on brain health is poorly understood. Astrocyte activation occurs in response to diverse insults, and plays a critical role in brain health and disease. We report that the core clock protein BMAL1 regulates astrogliosis in a synergistic manner via a cell-autonomous mechanism, and via a lesser non-cell-autonomous signal from neurons. Astrocyte-specific Bmal1 deletion induces astrocyte activation in vitro and in vivo, mediated in part by suppression of glutathione-s-transferase signaling. Functionally, loss of Bmal1 in astrocytes promotes neuronal death in vitro. Our results demonstrate that the core clock protein BMAL1 regulates astrocyte activation and function in vivo, elucidating a novel mechanism by which the circadian clock could influence many aspects of brain function and neurologic disease.HighlightsCircadian disruption promotes astrocyte activation.Astrocyte-specific deletion of the circadian clock gene BMAL1 induces astrocyte activation.BMAL1 regulates astrocyte activation by altering glutathione-s-transferase signaling.Loss of astrocyte BMAL1 enhances neuronal cell death in a co-culture system.eTOC blurbLananna et al. show that the circadian clock protein BMAL1 regulates astrocyte activation via a cell autonomous-mechanism involving diminished glutathione-s-transferase signaling. This finding elucidates a novel function of the core circadian clock in astrocytes, and reveals a BMAL1 as a modulator of astrogliosis.

Deubiquitinating enzyme USP9X regulates cellular clock function by modulating the ubiquitination and degradation of a core circadian protein BMAL1

2018 ◽  
Vol 475 (8) ◽  
pp. 1507-1522 ◽  
Author(s):  
Yang Zhang ◽  
Chunyan Duan ◽  
Jing Yang ◽  
Suping Chen ◽  
Qing Liu ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Circadian Clock ◽  
Clock Genes ◽  
Affinity Purification ◽  
Mass Spectrometry Analysis ◽  
Regulatory Function ◽  
Spectrometry Analysis ◽  
The Core ◽  
Clock Proteins ◽  
Clock Protein

Living organisms on the earth maintain a roughly 24 h circadian rhythm, which is regulated by circadian clock genes and their protein products. Post-translational modifications of core clock proteins could affect the circadian behavior. Although ubiquitination of core clock proteins was studied extensively, the reverse process, deubiquitination, has only begun to unfold and the role of this regulation on circadian function is not completely understood. Here, we use affinity purification and mass spectrometry analysis to identify probable ubiquitin carboxyl-terminal hydrolase FAF-X (USP9X) as an interacting protein of the core clock protein aryl hydrocarbon receptor nuclear translocator-like protein 1 (ARNTL or BMAL1). Through biochemical experiments, we discover that USP9X reduces BMAL1 ubiquitination, enhances its stability, and increases its protein level, leading to the elevated transcriptional activity. Bioluminescence measurement reveals that USP9X knockdown decreases the amplitude of the cellular circadian rhythm but the period and phase are not affected. Our experiments find a new regulator for circadian clock at the post-translational level and demonstrate a different regulatory function for the circadian clock through the deubiquitination and the up-regulation of the core clock protein BMAL1 in the positive limb of the transcription–translation feedback loop.

scholarly journals Selenium is a modulator of circadian clock that protects mice from the toxicity of a chemotherapeutic drug via upregulation of the core clock protein, BMAL1

Oncotarget ◽  
2011 ◽  
Vol 2 (12) ◽  
pp. 1279-1290 ◽  
Author(s):  
Yan Hu ◽  
Mary L. Spengler ◽  
Karen K. Kuropatwinski ◽  
Maria Comas-Soberats ◽  
Marilyn Jackson ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Chemotherapeutic Drug ◽  
The Core ◽  
Clock Protein
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