Alternative polyadenylation factor CPSF6 regulates temperature compensation of the mammalian circadian clock
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive HF
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Permanent Cell Line Cell
DISEASE(S): Osteosarcoma
SUBMITTER: 
Tanja Bange
LAB HEAD: Prof. Dr. Charo Robles
PROVIDER: PXD029343 | Pride | 2023-05-23
REPOSITORIES: Pride
Dataset's files
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| 20181231_TB_SA_Bert_prot_07.raw | Raw | |||
| 20181231_TB_SA_Bert_prot_08.raw | Raw | |||
| 20181231_TB_SA_Bert_prot_09.raw | Raw | |||
| 20181231_TB_SA_Bert_prot_10.raw | Raw | |||
| 20181231_TB_SA_Bert_prot_11.raw | Raw |
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Similar Datasets
Project description:Ambient temperature potentially affects all biological systems. However, the period length of circadian clocks is close to 24 h over a broad range of physiological temperatures, known as temperature compensation. The mechanism underpinning the temperature compensation remains largely unknown. Here, we show that inhibitors of time progression, TIMING OF CAB EXPRESSION 1 (TOC1) and PSEUDO-RESPONSE REGULATOR 5 (PRR5) proteins, are required for the temperature compensation in Arabidopsis thaliana (Arabidopsis). Compared to the wild-type, the prr5 toc1 double mutant shows a short period at high temperatures. TOC1 and PRR5 proteins are ubiquitinated and degraded at low temperatures, by a ubiquitin E3 ligase LOV KELCH PROTEIN 2 (LKP2) that was sought as a minor player in the clock. The lkp2 mutants show long periods only at lower temperatures. Collectively, the clock keeps its periodicity against ambient temperature by the temperature-dependent quantity control of inhibitors of time progression.
DOI:10.1126/sciadv.adq0187
2024-10-04 | PXD044813 | JPOST Repository
Project description:Daily (circadian) clocks are essential for regulating and coordinating physiology in mammals. Modulation of local chromatin structure has been shown for only a small number of genes, principally thought to be directly modulated by Clock-mediated histone acetylation. Here we show that genome-wide changes of active and suppressive histone marks control global chromatin architecture over the day and night. Examination of mouse liver tissue at 4 time-points around the clock in "free-running", continuous conditions (constant darkness, temperature and food available ad libitum).
2013-01-08 | E-GEOD-23550 | biostudies-arrayexpress
Project description:Circadian clocks drive ~24 hr rhythms in tissue physiology. They rely on transcriptional/translational feedback loops driven by interacting networks of clock complexes.To gain insights into the role of the mammary clock, circadian time-series microarrays were performed to identify rhythmic genes in vivo. Breast tissues were isolated at 4 hr intervals for two circadian (24 hourly) cycles, from mice kept under constant darkness to avoid any light- or dark-driven genes.
2017-12-01 | E-MTAB-5330 | biostudies-arrayexpress
Project description:Mammals rely on a network of circadian clocks to control daily systemic metabolism and physiology. The central pacemaker in the suprachiasmatic nucleus (SCN) is considered hierarchically dominant over peripheral clocks, whose degree of independence, or tissue-level autonomy, has never been ascertained in vivo. Using arrhythmic Bmal1-null mice, we generated animals with reconstituted circadian expression of BMAL1 exclusively in the liver (Liver-RE). High-throughput transcriptomics and metabolomics show that the liver has independent circadian functions specific for metabolic processes such as the NAD+ salvage pathway and glycogen turnover. However, although BMAL1 occupies chromatin at most genomic targets in Liver-RE mice, circadian expression is restricted to ∼10% of normally rhythmic transcripts. Finally, rhythmic clock gene expression is lost in Liver-RE mice under constant darkness. Hence, full circadian function in the liver depends on signals emanating from other clocks, and light contributes to tissue-autonomous clock function.
2019-06-13 | GSE132659 | GEO
Project description:Tseng2012 - Circadian clock of N.crassa
A comprehensive model of the circardian clock of fungal Neurospora crassa
, which encompasses existing knowledge of the biochemistry of Neurospora clock, is described by Tseng et al.
(2012). The model is validated against a wide range of experimental phenotypes and has been used to investigate possible molecular explanations of temperature compensation.
This model is described in the article:
Comprehensive modelling of the Neurospora circadian clock and its temperature compensation.
Tseng YY, Hunt SM, Heintzen C, Crosthwaite SK, Schwartz JM
PLoS Comput. Biol. [2012 ; Volume: 8 (Issue: 3 )] Page info: e1002437
Abstract:
Circadian clocks provide an internal measure of external time allowing organisms to anticipate and exploit predictable daily changes in the environment. Rhythms driven by circadian clocks have a temperature compensated periodicity of approximately 24 hours that persists in constant conditions and can be reset by environmental time cues. Computational modelling has aided our understanding of the molecular mechanisms of circadian clocks, nevertheless it remains a major challenge to integrate the large number of clock components and their interactions into a single, comprehensive model that is able to account for the full breadth of clock phenotypes. Here we present a comprehensive dynamic model of the Neurospora crassa circadian clock that incorporates its key components and their transcriptional and post-transcriptional regulation. The model accounts for a wide range of clock characteristics including: a periodicity of 21.6 hours, persistent oscillation in constant conditions, arrhythmicity in constant light, resetting by brief light pulses, and entrainment to full photoperiods. Crucial components influencing the period and amplitude of oscillations were identified by control analysis. Furthermore, simulations enabled us to propose a mechanism for temperature compensation, which is achieved by simultaneously increasing the translation of frq RNA and decreasing the nuclear import of FRQ protein.
Figure 3 of the reference publication has been reproduced using Copasi 4.8 (Build 35).
This model is hosted on BioModels Database
and identified
by: MODEL1212150000
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2024-09-02 | BIOMD0000000437 | BioModels
Project description:A defining property of circadian clocks is temperature compensation, characterized by the resilience of their near 24-hour free-running periods against changes in environmental temperature within the physiological range. While temperature compensation is evolutionary conserved across different taxa of life and has been studied within many model organisms, its molecular underpinnings remain elusive. Posttranscriptional regulations such as temperature-sensitive alternative splicing or phosphorylation have been described as underlying reactions. Here, we show that knockdown of cleavage and polyadenylation specificity factor subunit 6 (CPSF6), a key regulator of 3'-end cleavage and polyadenylation, significantly alters circadian temperature compensation in human U-2 OS cells. We apply a combination of 3'-end-RNA-seq and mass spectrometry-based proteomics to globally quantify changes in 3' UTR length as well as gene and protein expression between wild-type and CPSF6 knockdown cells and their dependency on temperature. Since changes in temperature compensation behavior should be reflected in alterations of temperature responses within one or all of the 3 regulatory layers, we statistically assess differential responses upon changes in ambient temperature between wild-type and CPSF6 knockdown cells. By this means, we reveal candidate genes underlying circadian temperature compensation, including eukaryotic translation initiation factor 2 subunit 1 (EIF2S1).
| S-EPMC10335657 | biostudies-literature
Project description:Gould2011 - Temperature Sensitive Circadian
Clock
This model is a temperature sensitive
version of Pokhilko
et al. 2010 (PMID:
20865009),
which is
BIOMD0000000273
in BioModels.
This model is described in the article:
Network balance via CRY
signalling controls the Arabidopsis circadian clock over
ambient temperatures.
Gould PD, Ugarte N, Domijan M, Costa
M, Foreman J, Macgregor D, Rose K, Griffiths J, Millar AJ,
Finkenstädt B, Penfield S, Rand DA, Halliday KJ, Hall
AJ.
Mol. Syst. Biol. 2013; 9: 650
Abstract:
Circadian clocks exhibit 'temperature compensation', meaning
that they show only small changes in period over a broad
temperature range. Several clock genes have been implicated in
the temperature-dependent control of period in Arabidopsis. We
show that blue light is essential for this, suggesting that the
effects of light and temperature interact or converge upon
common targets in the circadian clock. Our data demonstrate
that two cryptochrome photoreceptors differentially control
circadian period and sustain rhythmicity across the
physiological temperature range. In order to test the
hypothesis that the targets of light regulation are sufficient
to mediate temperature compensation, we constructed a
temperature-compensated clock model by adding passive
temperature effects into only the light-sensitive processes in
the model. Remarkably, this model was not only capable of full
temperature compensation and consistent with mRNA profiles
across a temperature range, but also predicted the
temperature-dependent change in the level of LATE ELONGATED
HYPOCOTYL, a key clock protein. Our analysis provides a
systems-level understanding of period control in the plant
circadian oscillator.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000564.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000564 | BioModels
Project description:The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver
2019-06-11 | GSE117134 | GEO
Project description:In mammals, circadian clocks are strictly suppressed during early embryonic stages as well as pluripotent stem cells, by the lack of CLOCK/BMAL1 mediated circadian feedback loops. During ontogenesis, the innate circadian clocks emerge gradually at a late developmental stage, then, with which the circadian temporal order is invested in each cell level throughout a body. Meanwhile, in the early developmental stage, a segmented body plan is essential for an intact developmental process and somitogenesis is controlled by another cell-autonomous oscillator, the segmentation clock, in the posterior presomitic mesoderm (PSM). In the present study, focusing upon the interaction between circadian key components and the segmentation clock, we investigated the effect of the CLOCK/BMAL1 on the segmentation clock Hes7 oscillation, revealing that the expression of functional CLOCK/BMAL1 severely interferes with the ultradian rhythm of segmentation clock in induced PSM and gastruloids. RNA sequencing analysis showed that the premature expression of CLOCK/BMAL1 affects the Hes7 transcription and its regulatory pathways. These results suggest that the suppression of CLOCK/BMAL1-mediated transcriptional regulation during the somitogenesis may be inevitable for intact mammalian development.
2021-12-09 | GSE181295 | GEO
Project description:Physiology is regulated by interconnected cell and tissue circadian clocks. Disruption of the rhythms generated by this interconnectedness is associated with metabolic disease. Here we tested the interactions between clocks in two critical components of organismal metabolism – liver and skeletal muscle – by rescuing clock function either in each organ separately, or in both organs simultaneously, in otherwise clock-less mice. Experiments revealed that individual clocks are partially sufficient for tissue glucose metabolism, yet the connections between both tissue clocks coupled with daily feeding rhythms maximizes systemic glucose tolerance. This synergy relies in part on local transcriptional control of the glucose machinery, feeding-responsive signals such as insulin, and metabolic cycles that connect the muscle and liver. We posit that spatiotemporal mechanisms of muscle and liver play an essential role in the maintenance of systemic glucose homeostasis, and that disrupting this diurnal coordination can contribute to the metabolic disease.
2023-05-29 | GSE228389 | GEO