Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4036610.fastq.gz | Fastqsanger.gz | |||
| SRR4036620.fastq.gz | Fastqsanger.gz | |||
| SRR4036630.fastq.gz | Fastqsanger.gz | |||
| SRR4036601.fastq.gz | Fastqsanger.gz | |||
| SRR4036611.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 33 |
Similar Datasets
Project description:Circadian rhythm in clock mutants
| PRJNA93919 | ENA
Project description:The daily pattern of temporal gene expression is regulated by the circadian clock system. Under constant environmental conditions, aging is associated with a shortening of the endogenous period of circadian rhythms in Arabidopsis. This study investigated to investigate how aging influences the waveforms of rhythmic patterns of gene expression under light/dark cycles. The waveforms of the daily cycling circadian clock showed significant warping in aged leaves, which shifted their expression pattern. Transcriptomic analysis revealed that the number of daily cycling genes in aged leaves was reduced by more than half. Furthermore, in aged plants, the expression schedule of cycling genes in both young and old leaves warped. Circadian clock mutants, including toc1, which did not exhibit age-dependent warping, had significantly altered warping patterns.
2023-12-05 | GSE248801 | GEO
Project description:Zhou2015 - Circadian clock with immune
regulator NPR1
Arabidopsis clock model modified from
P2012 (Pokhilko et al., 2013 -
BIOMD0000000445)
model to include the master immune regulator NPR1 coupling to LHY,
TOC1 and PRR7.
Triggers: The Global Quantities contain triggers that allow
one to change coupling settings, Salicyclic acid (SA) treatment and
npr1 mutants.
LHY_on: true->NPR1 couples to LHY
PRR7_on: true->NPR1 couples to PRR7
WT: true->WT plants, false->npr1 mutant plants
SA: true->SA treated plants, false->no treatment
This model has L=1, i.e. operates only under constant light
conditions and is not aiming to make preditions under diurnal
conditions. Due to period overshoot only time points after 28h are
relevant.
This model is described in the article:
Redox rhythm reinforces the
circadian clock to gate immune response.
Zhou M, Wang W, Karapetyan S, Mwimba
M, Marqués J, Buchler NE, Dong X.
Nature 2015 Jun;
Abstract:
Recent studies have shown that in addition to the
transcriptional circadian clock, many organisms, including
Arabidopsis, have a circadian redox rhythm driven by the
organism's metabolic activities. It has been hypothesized that
the redox rhythm is linked to the circadian clock, but the
mechanism and the biological significance of this link have
only begun to be investigated. Here we report that the master
immune regulator NPR1 (non-expressor of pathogenesis-related
gene 1) of Arabidopsis is a sensor of the plant's redox state
and regulates transcription of core circadian clock genes even
in the absence of pathogen challenge. Surprisingly, acute
perturbation in the redox status triggered by the immune signal
salicylic acid does not compromise the circadian clock but
rather leads to its reinforcement. Mathematical modelling and
subsequent experiments show that NPR1 reinforces the circadian
clock without changing the period by regulating both the
morning and the evening clock genes. This balanced network
architecture helps plants gate their immune responses towards
the morning and minimize costs on growth at night. Our study
demonstrates how a sensitive redox rhythm interacts with a
robust circadian clock to ensure proper responsiveness to
environmental stimuli without compromising fitness of the
organism.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000577.
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 | BIOMD0000000577 | BioModels
Project description:Study on differential gene expression and splicing between wildtype and clock mutants. This study is part of a comparative analysis of the role of Protein Methyltransferase 5 in the regulation of transcriptional and post-transcriptional processes simultaneously in Arabidopsis and Drosophila. Circadian rhythms allow organisms to time biological processes to the most appropriate phases of the day/night cycle1. Post-transcriptional regulation is emerging as an important component of circadian networks2-6, but the molecular mechanisms linking the circadian clock to the control of RNA processing are largely unknown. Here we show that Protein Arginine Methyl Transferase 5 (PRMT5), which transfers methyl groups to arginine residues present in histones7 and Sm spliceosomal proteins8,9, links the circadian clock to the control of alternative splicing in plants. Mutations in prmt5impair multiple circadian rhythms in Arabidopsis thaliana and this phenotype is caused, at least in part, by a strong alteration in alternative splicing of the core-clock gene PSEUDO RESPONSE REGULATOR 9 (PRR9). Furthermore, genome wide studies show that PRMT5 contributes to regulate many pre-mRNA splicing events most likely modulating 5´splice site (5´ss) recognition. PRMT5 expression shows daily and circadian oscillations, and this contributes to mediate the circadian regulation of expression and alternative splicing of a subset of genes. Circadian rhythms in locomotor activity are also disrupted in dart5, a mutant affected in the Drosophila melanogaster PRMT5 homolog, and this is associated with alterations in splicing of the core-clock gene period (per) and several clock associated genes. Our results reveal a key role for PRMT5 in the regulation of alternative splicing and indicate that the interplay between the circadian clock and the regulation of alternative splicing by PRMT5 constitutes a common mechanism that helps organisms to synchronize physiological processes with daily changes in environmental conditions.
2010-08-24 | GSE18808 | GEO
Project description:Circadian pace is modulated by light intensity, known as the Aschoff’s rule, with largely unrevealed mechanisms. Here we report that photoreceptor CRY2 mediates blue light input to circadian clock by directly interacting with clock core component PRR9 in blue light dependent manner. This physical interaction dually blocks the accessibility of PRR9 protein to its co-repressor TPL/TPRs and the resulting kinase PPKs. Notably, phosphorylation of PRR9 by PPKs is critical for its DNA binding and repressive activity, hence to ensure proper circadian speed. Given the labile nature of CRY2 in strong blue light, our findings provide a mechanistic explanation for Aschoff’s rule in plants, i.e., blue light triggers CRY2 turnover in proportional to its intensity, which accordingly releasing PRR9 to fine tune circadian speed. Our findings not only reveal a novel network mediating light input into circadian clock, but also unmask a mechanism by which Arabidopsis circadian clock sensing light intensity.
2022-10-06 | PXD035252 | 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