Ontology highlight
ABSTRACT:
PROVIDER: PRJNA415418 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6202910_1.fastq.gz | Fastqsanger.gz | |||
| SRR6202910_2.fastq.gz | Fastqsanger.gz | |||
| SRR6202911_1.fastq.gz | Fastqsanger.gz | |||
| SRR6202911_2.fastq.gz | Fastqsanger.gz | |||
| SRR6202912_1.fastq.gz | Fastqsanger.gz |
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Project description:We observe the increase of stress resilience in Drosophila in which the m6A methyltransferase Mettl3 is knocked down. Mettl3-dependent m6A is present in the 5' UTR of genes enriched for neurogenesis and signaling pathways, and determine that Mettl3-dependent m6A regulates the decay of heat shock chaperones. Expression levels of genes with Mettl3-dependent m6A are increased with the reduction of Mettl3 and with heat shock stress in the brain.
2022-08-26 | GSE178955 | GEO
Project description:Some individuals show a discrepancy between cognition and the amount of neuropathological changes characteristic for Alzheimer’s disease (AD). This phenomenon has been referred to as ‘resilience’. The molecular and cellular underpinnings of resilience remain poorly understood. To obtain an unbiased understanding of the molecular changes underlying resilience, we investigated global changes in gene expression in the superior frontal gyrus of a cohort of cognitively and pathologically well-defined AD patients, resilient individuals and age-matched controls (n=11-12 per group). 897 genes were significantly altered between AD and control, 1121 between resilient and control and 6 between resilient and AD. Gene set enrichment analysis (GSEA) revealed that the expression of metallothionein (MT) and of genes related to mitochondrial processes was higher in the resilient donors. Weighted gene co-expression network analysis (WGCNA) identified gene modules related to the unfolded protein response, mitochondrial processes and synaptic signaling to be differentially associated with resilience or dementia. As changes in MT, mitochondria, heat shock proteins and the unfolded protein response (UPR) were the most pronounced changes in the GSEA and/or WGCNA, immunohistochemistry was used to further validate these processes. MT was significantly increased in astrocytes in resilient individuals. A higher proportion of the mitochondrial gene MT-CO1 was detected outside the cell body versus inside the cell body in the resilient compared to the control group and there were higher levels of heat shock protein 70 (HSP70) and X-box-binding protein 1 spliced (XBP1s), two proteins related to heat shock proteins and the UPR, in the AD donors. Finally, we show evidence for putative sex-specific alterations in resilience, including gene expression differences related to autophagy in females compared to males. Taken together, these results show possible mechanisms involving MTs, mitochondrial processes and the UPR by which individuals might maintain cognition despite the presence of AD pathology.
2024-04-25 | GSE261817 | GEO
Project description:Mutants of the Mnn1 gene are hyper-sensitive to several stresses and display increased genome instability when subjected to conditions, such as heat shock, generally regarded as non-genotoxic. We describe a role for Menin as a global regulator of heat shock gene expression and critical factor in the maintenance of genome integrity 2-colour microarray design using 36 microarrays testing shock vs non shock in Drosophila melanogaster. Using a test of loss-of-heterozygosity, we show that Drosophila strains lacking a functional Mnn1 gene or expressing a Mnn1 dsRNAi are characterized by increased genome instability in response to short, repeated but non-lethal heat shock or hypoxia treatments. The same was true for strains lacking all Hsp70 genes.
2010-10-25 | E-GEOD-20497 | biostudies-arrayexpress
Project description:We performed ChIP-seq of Hsf1 under non heat shock, 5-minute heat shock and 120 minute heat shock conditions. We used the conditional chemical genetics approach known as “anchor away” (AA) to rapidly inactivate Hsf1. We coupled Hsf1-AA to and nascent RNA seq (NAC)-seq to define the genes whose expression depends on Hsf1 during heat shock.
2018-07-26 | GSE117653 | GEO
Project description:We utilized chromatin immunoprecipitation sequencing (ChIP-seq) to analyze the binding of HSF1 and HSF2 to chromatin under oxidative stress and heat shock. ChIP-seq was performed in mouse embryonic fibroblasts (MEFs) that were exposed to heat shock (HS) or oxidative stress induced by menadione (MD). Antibodies against HSF1 and HSF2 were used for immunoprecipitation.
2022-06-10 | GSE183244 | GEO
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7.
2015-02-20 | GSE57397 | GEO
Project description:In this study we perform precision nuclear run-on sequencing (PRO-seq) to measure the altered transcriptional response upon CDK7 inhibition or RNA-seq to elucidate the response of CDK7 inhibition on steady-state RNA. We performed a heat shock time course in PRO-seq with and without the Syros CDK7 inhibitor SY5609. Matching this data we performed three deeply sequenced RNA-seq experiments with SY5609 that include no heat shock, heat shock with recovery and long heat shock with no recovery. We additionally generated two more RNA-seq datasets in heat shock conditions with another Syros inhibitor, SY5102 and in a CDK7-analog sensitive OV90 cell line treated with 3MBPP1.
2024-12-19 | GSE228346 | GEO
Project description:Environmental conditions are quite effective during propagation and industrial application of Baker’s yeast (Saccharomyces cerevisiae). The change of temperature is one of the most important conditions which affects the dough-leaving capacity of yeast cells. Accordingly, heat changes play an essential role in the commercial and economic impact of the yeast. Recent technologies in genomics have been used for analysis of global gene expression profiles such as microarray and RNA sequencing to solve the problems related with industrial application of yeast. Hereby, the aim of this study is to explore the effects of heat stresses on global gene expression profiles and to identify the candidate genes for the heat stress response in commercial baker’s yeast by using microarray technology and comparative statistical data analyses. Data from all hybridizations and array normalization were analyzed using the GeneSpringGX 12.1 (Agilent) and the R 2.15.2 program language. In the analysis of this dataset, all required statistical methods are performed comparatively in each step and the best performed ones are used in further computations. Hence, as the first step of the analyses, different background normalization algorithms such as MAS5.0, RMA, MBEI and GC-RMA were applied and the algorithm which gives the most accurate findings was chosen for the normalization procedure. As a result, expression values, computed from CEL files, were processed by Robust Multiarray Analysis (RMA) which is the selected procedure for the normalization of the systematic differences between samples. In order to determine differentially expressed genes under heat stress treatments, two different methods, namely, the fold-change and the hypothesis testing approaches are executed. In the fold-change method, various cut-off values are implemented while different multiple testing procedures are performed for the hypothesis testing. Under the heat shock and temperature-shift stress conditions, up/down regulated differentially expressed probes were functionally categorized into the different groups via the cluster analyses. Transcriptome changes under the heat shock and temperature-shift stress treatments show that the number of differentially up-regulated genes among the heat shock proteins (HSPs) and transcription factors (TFs) changed significantly. Consequently, the identification of thousands of genes related with heat stress treatments via microarray technology and comparative statistical analysis resulted in the creation of big picture which provides the understanding of the importance for the baker’s yeast industrial applications.
2017-01-30 | E-MTAB-3459 | biostudies-arrayexpress
Project description:Proctor2005 - Actions of chaperones and their
role in ageing
This model is described in the article:
Modelling the actions of
chaperones and their role in ageing.
Proctor CJ, Soti C, Boys RJ,
Gillespie CS, Shanley DP, Wilkinson DJ, Kirkwood TB.
Mech. Ageing Dev. 2005 Jan; 126(1):
119-131
Abstract:
Many molecular chaperones are also known as heat shock
proteins because they are synthesised in increased amounts
after brief exposure of cells to elevated temperatures. They
have many cellular functions and are involved in the folding of
nascent proteins, the re-folding of denatured proteins, the
prevention of protein aggregation, and assisting the targeting
of proteins for degradation by the proteasome and lysosomes.
They also have a role in apoptosis and are involved in
modulating signals for immune and inflammatory responses.
Stress-induced transcription of heat shock proteins requires
the activation of heat shock factor (HSF). Under normal
conditions, HSF is bound to heat shock proteins resulting in
feedback repression. During stress, cellular proteins undergo
denaturation and sequester heat shock proteins bound to HSF,
which is then able to become transcriptionally active. The
induction of heat shock proteins is impaired with age and there
is also a decline in chaperone function. Aberrant/damaged
proteins accumulate with age and are implicated in several
important age-related conditions (e.g. Alzheimer's disease,
Parkinson's disease, and cataract). Therefore, the balance
between damaged proteins and available free chaperones may be
greatly disturbed during ageing. We have developed a
mathematical model to describe the heat shock system. The aim
of the model is two-fold: to explore the heat shock system and
its implications in ageing; and to demonstrate how to build a
model of a biological system using our simulation system
(biology of ageing e-science integration and simulation
(BASIS)).
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000091.
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 | BIOMD0000000091 | BioModels
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels