An integrative omics approach reveals posttranscriptional mechanisms underlying circadian temperature compensation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA771183 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16324725.fastq.gz | Fastqsanger.gz | |||
| SRR16324726.fastq.gz | Fastqsanger.gz | |||
| SRR16324727.fastq.gz | Fastqsanger.gz | |||
| SRR16324728.fastq.gz | Fastqsanger.gz | |||
| SRR16324729.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:We apply 3'-End-RNA-seq based sequencing to globally quantify polyadenylation sites and transcript isoform abundance in human U-2 OS cells under wild-type and CPSF6 knock-down conditions at 3 different temperatures (32°C, 37°C and 39°C). We show that CPSF6 knock-down as well as temperature alterations lead to global changes in 3' UTR length and transcript abundance. By means of a differential response analysis with respect to temperature changes in wild type and temperature-decompensated CPSF6 knockdown cells, we reveal candidate genes underlying circadian temperature compensation.
2023-05-31 | GSE185896 | GEO
Project description:A defining property of circadian clocks is temperature compensation, characterized by the resilience of circadian free-running periods against changes in environmental temperature.We quantify global changes in 3´UTR length as well as gene and protein expression between wild type and CPSF6 knock-down cells and their dependency on temperature.
2023-05-23 | PXD029343 | Pride
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: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:A temperature independent period and temperature entrainment are two defining features of circadian oscillators. A default model of distributed temperature compensation satisfies these basic facts yet is not easily reconciled with other properties of circadian clocks, such as many mutants with altered but temperature compensated periods. The default model also suggests that the shape of the circadian limit cycle and the associated phase response curves (PRC) will vary since the average concentrations of clock proteins change with temperature. We propose an alternative class of models where the twin properties of a fixed period and entrainment are structural and arise from an underlying adaptive system that buffers temperature changes. These models are distinguished by a PRC whose shape is temperature independent and orbits whose extrema are temperature independent. They are readily evolved by local, hill climbing, optimization of gene networks for a common quality measure of biological clocks, phase anticipation. Interestingly a standard realization of the Goodwin model for temperature compensation displays properties of adaptive rather than distributed temperature compensation.
| S-EPMC3395600 | biostudies-literature
Project description:The internal circadian rhythms of cells and organisms coordinate their physiological properties to the prevailing 24-h cycle of light and dark on earth. The mechanisms generating circadian rhythms have four defining characteristics: they oscillate endogenously with period close to 24 h, entrain to external signals, suffer phase shifts by aberrant pulses of light or temperature, and compensate for changes in temperature over a range of 10 degrees C or more. Most theoretical descriptions of circadian rhythms propose that the underlying mechanism generates a stable limit cycle oscillation (in constant darkness or dim light), because limit cycles quite naturally possess the first three defining properties of circadian rhythms. On the other hand, the period of a limit cycle oscillator is typically very sensitive to kinetic rate constants, which increase markedly with temperature. Temperature compensation is therefore not a general property of limit cycle oscillations but must be imposed by some delicate balance of temperature dependent effects. However, "delicate balances" are unlikely to be robust to mutations. On the other hand, if circadian rhythms arise from a mechanism that concentrates sensitivity into a few rate constants, then the "balancing act" is likely to be more robust and evolvable. We propose a switch-like mechanism for circadian rhythms that concentrates period sensitivity in just two parameters, by forcing the system to alternate between a stable steady state and a stable limit cycle.
| S-EPMC1773060 | biostudies-literature
Project description:Purpose: Circadian clock in plants temporally coordinates biological processes throughout the day synchronizing gene expression with environmental changes. Here, we examined the genome-wide circadian and diurnal control of Arabidopsis transcriptome using high throughout RNA-seq approach. Methods: Transcriptional and posttranscritional profiles were identified and characterized for Arabidopsis seedlings grown under continuous light or long-day condition (16 h light/8 h dark) for one day (each condition has two biological replicates). Results: We show that rhythmic posttranscriptional regulation is also a significant factor for genome-wide profile of circadian plant transcriptome. Two major posttranscriptioal mechanisms alternative splicing (AS) and alternative polyadenylation (APA) show circadian rhythmicity, resulting from the oscillation in the genes invovled in AS and APA. Conclusions: Arabidopsis circadian clock not only controls the transcription of genes, but also affects their posttranscriptional regulation through regulating AS and APA.
2020-01-14 | GSE137732 | GEO
Project description:Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for the clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here we report that a conserved SNW/SKIP domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in the posttranscriptional regulation of circadian clock genes in Arabidopsis. Mutation in SKIP lengthens the circadian period in a temperature sensitive manner, affects light input and the sensitivity of light resetting to the clock. SKIP physically interacts with the spliceosomal splicing factor SR45 and associates with the pre-mRNA of clock genes, such as PRR7 and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splicing site. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock functions at a posttranscriptional level. Our findings revealed that AtSKIP is a splicing factor and a component of spliceosome. To further investigate effects of mutation in SKIP on the genome-wide changes of alternative splicing, we performed ultra-highthroughput RNA sequencing, using 10-day old seedlings. Two biological replicates for both wild type (Col-0) and skip-2 were designed.
2012-12-13 | E-GEOD-32216 | biostudies-arrayexpress
Project description:Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for the clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here we report that a conserved SNW/SKIP domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in the posttranscriptional regulation of circadian clock genes in Arabidopsis. Mutation in SKIP lengthens the circadian period in a temperature sensitive manner, affects light input and the sensitivity of light resetting to the clock. SKIP physically interacts with the spliceosomal splicing factor SR45 and associates with the pre-mRNA of clock genes, such as PRR7 and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splicing site. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock functions at a posttranscriptional level.
2012-12-13 | GSE32216 | GEO
Project description:Posttranscriptional mRNA expression changes in stress
| PRJEB9446 | ENA