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#33859007   // To Up

Comment on "Circadian rhythms in the absence of the clock gene ".

Ray (Reports, 14 February 2020, p. 800) report apparent transcriptional circadian rhythms in mouse tissues lacking the core clock component BMAL1. To better understand these surprising results, we reanalyzed the associated data. We were unable to reproduce the original findings, nor could we identify reliably cycling genes. We conclude that there is insufficient evidence to support circadian transcriptional rhythms in the absence of .
Elan Ness-Cohn, Ravi Allada, Rosemary Braun

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Response to Comment on "Circadian rhythms in the absence of the clock gene ".

Abruzzi argue that transcriptome oscillations found in our study in the absence of are of low amplitude, statistical significance, and consistency. However, their conclusions rely solely on a different statistical algorithm than we used. We provide statistical measures and additional analyses showing that our original analyses and observations are accurate. Further, we highlight independent lines of evidence indicating -independent 24-hour molecular oscillations.
Sandipan Ray, Utham K Valekunja, Alessandra Stangherlin, Steven A Howell, Ambrosius P Snijders, Gopinath Damodaran, Akhilesh B Reddy

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#33859002   // To Up

Response to Comment on "Circadian rhythms in the absence of the clock gene ".

Ness-Cohn claim that our observations of transcriptional circadian rhythms in the absence of the core clock gene in mouse skin fibroblast cells are supported by inadequate evidence. They claim that they were unable to reproduce some of the original findings with their reanalysis. We disagree with their analyses and outlook.
Sandipan Ray, Utham K Valekunja, Alessandra Stangherlin, Steven A Howell, Ambrosius P Snijders, Gopinath Damodaran, Akhilesh B Reddy

2926 related Products with: Response to Comment on "Circadian rhythms in the absence of the clock gene ".

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#33859000   // To Up

Comment on "Circadian rhythms in the absence of the clock gene ".

Ray (Reports, 14 February 2020, p. 800) recently claimed temperature-compensated, free-running mRNA oscillations in liver slices and skin fibroblasts. We reanalyzed these data and found far fewer reproducible mRNA oscillations in this genotype. We also note errors and potentially inappropriate analyses.
Katharine C Abruzzi, Cédric Gobet, Felix Naef, Michael Rosbash

1826 related Products with: Comment on "Circadian rhythms in the absence of the clock gene ".

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#33641746   2020/12/07 To Up

Genomic perspectives on the circadian clock hypothesis of psychiatric disorders.

Circadian rhythm disturbances are frequently described in psychiatric disorders such as major depressive disorder, bipolar disorder, and schizophrenia. Growing evidence suggests a biological connection between mental health and circadian rhythmicity, including the circadian influence on brain function and mood and the requirement for circadian entrainment by external factors, which is often impaired in mental illness. Mental (as well as physical) health is also adversely affected by circadian misalignment. The marked interindividual differences in this combined susceptibility, in addition to the phenotypic spectrum in traits related both to circadian rhythms and mental health, suggested the possibility of a shared genetic background and that circadian clock genes may also be candidate genes for psychiatric disorders. This hypothesis was further strengthened by observations in animal models where clock genes had been knocked out or mutated. The introduction of genome-wide association studies (GWAS) enabled hypothesis-free testing. GWAS analysis of chronotype confirmed the prominent role of circadian genes in these phenotypes and their extensive polygenicity. However, in GWAS on psychiatric traits, only one clock gene, ARNTL (BMAL1) was identified as one of the few loci differentiating bipolar disorder from schizophrenia, and macaque monkeys where the ARNTL gene has been knocked out display symptoms similar to schizophrenia. Another lesson from genomic analyses is that chronotype has an important genetic correlation with several psychiatric disorders and that this effect is unidirectional. We conclude that the effect of circadian disturbances on psychiatric disorders probably relates to modulation of rhythm parameters and extend beyond the core clock genes themselves.
Malcolm von Schantz, Mario A Leocadio-Miguel, Michael J McCarthy, Sergi Papiol, Dominic Landgraf

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#33630038   2021/02/25 To Up

The circadian clock: a central mediator of cartilage maintenance and osteoarthritis development?

The circadian clock is a specialised cell signalling pathway present in all cells. Loss of clock function leads to tissue degeneration and premature aging in animal models demonstrating the fundamental importance of clocks for cell, tissue and organism health There is now considerable evidence that the chondrocyte circadian clock is altered in osteoarthritis (OA). The purpose of this review is to summarise current knowledge regarding the nature of the change in the chondrocyte clock in OA and the implications of this change for disease development. Expression of the core clock component, BMAL1, has consistently been shown to be lower in OA chondrocytes. This may contribute to changes in chondrocyte differentiation and extracellular matrix turnover in disease. Circadian clocks are highly responsive to environmental factors. Mechanical loading, diet, inflammation and oxidative insult can all influence clock function. These factors may contribute to causing the change in the chondrocyte clock in OA.
Raewyn C Poulsen, James I Hearn, Nicola Dalbeth

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#33452240   2021/01/15 To Up

Rhythmic glucose metabolism regulates the redox circadian clockwork in human red blood cells.

Circadian clocks coordinate mammalian behavior and physiology enabling organisms to anticipate 24-hour cycles. Transcription-translation feedback loops are thought to drive these clocks in most of mammalian cells. However, red blood cells (RBCs), which do not contain a nucleus, and cannot perform transcription or translation, nonetheless exhibit circadian redox rhythms. Here we show human RBCs display circadian regulation of glucose metabolism, which is required to sustain daily redox oscillations. We found daily rhythms of metabolite levels and flux through glycolysis and the pentose phosphate pathway (PPP). We show that inhibition of critical enzymes in either pathway abolished 24-hour rhythms in metabolic flux and redox oscillations, and determined that metabolic oscillations are necessary for redox rhythmicity. Furthermore, metabolic flux rhythms also occur in nucleated cells, and persist when the core transcriptional circadian clockwork is absent in Bmal1 knockouts. Thus, we propose that rhythmic glucose metabolism is an integral process in circadian rhythms.
Ratnasekhar Ch, Guillaume Rey, Sandipan Ray, Pawan K Jha, Paul C Driscoll, Mariana Silva Dos Santos, Dania M Malik, Radoslaw Lach, Aalim M Weljie, James I MacRae, Utham K Valekunja, Akhilesh B Reddy

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96 tests1 Unit1.00 flask 100 UG50 mg100 extractions1 mg1.00 flask100 ml.10 ug96 assays

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Systematic analysis of differential rhythmic liver gene expression mediated by the circadian clock and feeding rhythms.

The circadian clock and feeding rhythms are both important regulators of rhythmic gene expression in the liver. To further dissect the respective contributions of feeding and the clock, we analyzed differential rhythmicity of liver tissue samples across several conditions. We developed a statistical method tailored to compare rhythmic liver messenger RNA (mRNA) expression in mouse knockout models of multiple clock genes, as well as PARbZip output transcription factors (//). Mice were exposed to ad libitum or night-restricted feeding under regular light-dark cycles. During ad libitum feeding, genetic ablation of the core clock attenuated rhythmic-feeding patterns, which could be restored by the night-restricted feeding regimen. High-amplitude mRNA expression rhythms in wild-type livers were driven by the circadian clock, but rhythmic feeding also contributed to rhythmic gene expression, albeit with significantly lower amplitudes. We observed that and / knockouts differed in their residual rhythmic gene expression. Differences in mean expression levels between wild types and knockouts correlated with rhythmic gene expression in wild type. Surprisingly, in PARbZip knockout mice, the mean expression levels of PARbZip targets were more strongly impacted than their rhythms, potentially due to the rhythmic activity of the D-box-repressor NFIL3. Genes that lost rhythmicity in PARbZip knockouts were identified to be indirect targets. Our findings provide insights into the diurnal transcriptome in mouse liver as we identified the differential contributions of several core clock regulators. In addition, we gained more insights on the specific effects of the feeding-fasting cycle.
Benjamin D Weger, Cédric Gobet, Fabrice P A David, Florian Atger, Eva Martin, Nicholas E Phillips, Aline Charpagne, Meltem Weger, Felix Naef, Frédéric Gachon

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