Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB15412 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR450847_1.fastq.gz | Fastqsanger.gz | |||
| DRR450847_2.fastq.gz | Fastqsanger.gz | |||
| DRR450848_1.fastq.gz | Fastqsanger.gz | |||
| DRR450848_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:LHT1/MAC7 contributes to proper alternative splicing under long-term heat stress and mediates the variation in the tolerance of Arabidopsis
| PRJDB15607 | ENA
Project description:Heat stress seriously affects the plant development and growth. Increasing evidence points to RNA splicing as co-transcriptional regulations linking heat stresses in plants. However, the mechanism of how heat stress trigger and affect alternative splicing (AS) events through crucial splicing factors is still not clear. Here, we discovered a heat stress-enhancing AS suppression involved in splicing factor SR45a function, whereby SR45a modulates automatic self regulation by strengthen the full length mRNA processing together with CBP20. A SR45a intron splicing–dependent luciferase transgenic line was generated to monitor the intron 4 splicing events. We determined that luciferase activity increases upon heat treatment due to the intron remove, which inhibits the production of SR45a splicing variants. Loss functions of SR45a rendered plants more sensitive to heat stress, whereas overexpresion full length SR45a expression enhanced their tolerance. Full length SR45a is Essential for heat-responsive gene expression and splicing. Interestingly, SR45a modulate self-splicing regulation through branch point recognition together with CBP20. Genetic and molecular experiments identified the CBP20 is a positive regulator under heat stress. In addition, we demonstrate that HSFA2 affects the transcriptional levels of SR45a to act upsteam of SR45a by directly binding SR45a promoter. Our research highlights the heat-responsive self-splicing regulation of SR45a as a novel feedback to enhance plant stress tolerance.
2024-11-30 | GSE248817 | GEO
Project description:Patterns of alternative splicing during heat stress in Arabidopsis thaliana and Boechera depauperata indicate complex and species-specific interactions between differential expression and alternative splicing.
2018-03-21 | GSE107820 | GEO
Project description:Arabidopsis MOS4-associated complex promotes microRNA biogenesis and pre-mRNA splicing
| PRJNA401314 | ENA
Project description:Over the past several decades, corals worldwide have been affected by global warming, experiencing severe bleaching events that have often lead to coral death. The symbiotic Red Sea coral Stylophora pistillata is considered an opportunistic ‘r’ strategist, thriving in relatively unstable and unpredictable environments, and it is considered a stress-tolerant species. This study aimed to examine S. pistillata gene expression and to clarify the cellular pathways that are active during short-term heat stress caused by an increase from 24°C to 34°C over a 10-day period. Total RNA was extracted from heat-stressed coral fragments, labeled and hybridized against a designated S. pistillata custom microarray containing approximately 12,000 genes. Our results show that the heat stress reaction was sighted from 32°C and intensified significantly after 34°C treatment. Protein interaction networks of up- and down-regulated genes were constructed. The main clustering groups of up-regulated genes were ER stress and ER protein folding, cell cycle, ubiquitin-mediated proteolysis, cell death and cell death regulation and cellular stress response genes. These genes were enriched in cellular pathways related to the unfolded protein response (UPR) in the ER, ER-associated degradation (ERAD) and ubiquitin-mediated proteolysis. An analysis of the down-regulated genes yielded different clusters of genes related to extracellular matrix and actin organization, collagen, negative regulation of cell death and the Notch and Wnt signaling pathways. Genes encoding redox regulation proteins and molecular chaperones may be considered accurate “early warning genes”, while genes related to sensing and repairing DNA damage are severe heat-related genes. Here, we suggest that during short-term heat stress, S. pistillata might divert cellular energy into mechanisms such as UPR and ERAD at the expense of growth and biomineralization processes in an effort to recover from the stress.
2014-12-22 | GSE47779 | GEO
Project description:Global warming has great impacts on plant growth and development. Heat shock transcription factors are the master regulators of heat stress response to alleviate protein misfolding in the cytosol in plants. However, how plants deal with accumulation of misfolded proteins in the endoplasmic reticulum (ER) under heat stress conditions is less understood, especially in crops such as in rice. Here we report a positive feed-back loop mediated by the membrane-associated transcription factors NTL3 and bZIP74 in heat stress response in rice. In response to heat stress, the ER-membrane-associated bZIP74 is activated and up-regulate the expression of NTL3 in rice; NTL3 encodes an ER-membrane-associated transcription factor that is activated and regulate downstream genes including bZIP74 involved in protein folding and reactive oxygen species scavenging. Loss-of-function mutations of NTL3 are sensitive to heat stress while inducible expression of the processed form of NTL3 increases heat stress tolerance in rice seedlings. Our work reveals the important role of NTL3 in ER stress response for heat stress tolerance in rice.
2020-04-20 | GSE122021 | GEO
Project description:Erguler2013 - Unfolded protein stress response
The model investigates the mechanism by which UPR (unfolded protein response) outcome switches between survival and death.
This model is described in the article:
A mathematical model of the unfolded protein stress response reveals the decision mechanism for recovery, adaptation and apoptosis.
Erguler K, Pieri M, Deltas C.
BMC Syst Biol. 2013 Feb 21;7(1):16.
Abstract:
BACKGROUND: The unfolded protein response (UPR) is a major signalling cascade acting in the quality control ofprotein folding in the endoplasmic reticulum (ER). The cascade is known to play an accessory rolein a range of genetic and environmental disorders including neurodegenerative and cardiovasculardiseases, diabetes and kidney diseases. The three major receptors of the ER stress involved withthe UPR, i.e. IRE1a, PERK and ATF6, signal through a complex web of pathways to convey anappropriate response. The emerging behaviour ranges from adaptive to maladaptive depending on theseverity of unfolded protein accumulation in the ER; however, the decision mechanism for the switchand its timing have so far been poorly understood.
RESULTS:
Here, we propose a mechanism by which the UPR outcome switches between survival and death.We compose a mathematical model integrating the three signalling branches, and perform a comprehensivebifurcation analysis to investigate possible responses to stimuli. The analysis reveals threedistinct states of behaviour, low, high and intermediate activity, associated with stress adaptation, tolerance,and the initiation of apoptosis. The decision to adapt or destruct can, therefore, be understoodas a dynamic process where the balance between the stress and the folding capacity of the ER playsa pivotal role in managing the delivery of the most appropriate response. The model demonstratesfor the first time that the UPR is capable of generating oscillations in translation attenuation and theapoptotic signals, and this is supplemented with a Bayesian sensitivity analysis identifying a set ofparameters controlling this behaviour.
CONCLUSIONS:
This work contributes largely to the understanding of one of the most ubiquitous signalling pathwaysinvolved in protein folding quality control in the metazoan ER. The insights gained have direct consequenceson the management of many UPR-related diseases, revealing, in addition, an extended listof candidate disease modifiers. Demonstration of stress adaptation sheds light to how preconditioningmight be beneficial in manifesting the UPR outcome to prevent untimely apoptosis, and paves the wayto novel approaches for the treatment of many UPR-related conditions.
In the paper, PERKA refers to the amount of phosphorylated PERK monomer. However, it refers to the active complex in the model. The complex with the model parameterization is formed of 4 monomers (n=4). So, the value of PERKA should be multiplied by 4, in order to generate the figures in the paper (eg. Figure 12).
An additional parameter (tmr=10)) is used in the model. This parameter is not mentioned in the paper. The model values of kf(=10) and kr(=1) are not consistent with that of the paper (kf=100, kr=10, in the paper). However, this is corrected by the introduction of "tmr" in the model, which is multiplied with kf and kr to get the resulting values.
The term "tmr" was missing in the kinetic laws of the reactions reu7 and reu8, in the original model. This has been corrected as per the author's request.
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2024-09-02 | BIOMD0000000446 | BioModels
Project description:During heat stress cyto-protective genes including heat shock proteins are transcriptionally up-regulated and post-transcriptional splicing is inhibited. In contrast, co-transcriptional mRNA-splicing is maintained. These factors closely resemble the proteotoxic stress response during tumor development. The bromodomain protein BRD4 has been identified as an integral member of the oxidative stress as well as of the inflammatory response. Furthermore, there is evidence for BRD4's role in splicing regulation; Using RNA-Seq analyses we indeed found a significant increase in splicing inhibition, in particular intron retentions, during heat treatment in BRD4-deficient cells, but not under normal conditions. Subsequent experiments revealed that heat stress leads to the recruitment of BRD4 to nuclear stress bodies, to the interaction with the heat shock factor 1 (HSF1) and to the transcriptional up-regulation of non-coding Sat III RNA transcripts. These findings implicate BRD4 as a central regulator of splicing during heat stress. Since BRD4 is a potent target for anti-cancer therapies, our data linking BRD4 to the splicing machinery and the heat stress response - give additional insight into the mode of action of BRD4 inhibitors. WI38 cells have been treated by heatshock and anti BRD4 siRNA and combination.
2016-09-07 | E-GEOD-73471 | biostudies-arrayexpress
Project description:During heat stress cyto-protective genes including heat shock proteins are transcriptionally up-regulated and post-transcriptional splicing is inhibited. In contrast, co-transcriptional mRNA-splicing is maintained. These factors closely resemble the proteotoxic stress response during tumor development. The bromodomain protein BRD4 has been identified as an integral member of the oxidative stress as well as of the inflammatory response. Furthermore, there is evidence for BRD4's role in splicing regulation; Using RNA-Seq analyses we indeed found a significant increase in splicing inhibition, in particular intron retentions, during heat treatment in BRD4-deficient cells, but not under normal conditions. Subsequent experiments revealed that heat stress leads to the recruitment of BRD4 to nuclear stress bodies, to the interaction with the heat shock factor 1 (HSF1) and to the transcriptional up-regulation of non-coding Sat III RNA transcripts. These findings implicate BRD4 as a central regulator of splicing during heat stress. Since BRD4 is a potent target for anti-cancer therapies, our data linking BRD4 to the splicing machinery and the heat stress response - give additional insight into the mode of action of BRD4 inhibitors.
2016-09-07 | GSE73471 | GEO
Project description:Analysis of the coordinated transcriptional reponse to heat shock and ER stress mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing, in triplicate, using Illumina HiSeq. The samples were collected from indicated timepoints after exposed to either heat stress or ER stress.
2015-09-04 | E-GEOD-65636 | biostudies-arrayexpress