Ontology highlight
ABSTRACT:
PROVIDER: PRJNA575570 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10222625.fastq.gz | Fastqsanger.gz | |||
| SRR10222626.fastq.gz | Fastqsanger.gz | |||
| SRR10222627.fastq.gz | Fastqsanger.gz | |||
| SRR10222628.fastq.gz | Fastqsanger.gz | |||
| SRR10222629.fastq.gz | Fastqsanger.gz |
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Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to infection with Flock House virus (FHV).
2009-04-01 | GSE15466 | GEO
Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to Flock House virus (FHV) replicon induction.
2009-04-01 | GSE15467 | GEO
Project description:Post-embryonic plant development must be coordinated in response to and with environmental feedback. Development of above-ground organs is orchestrated from stem cells in the center of the shoot apical meristem (SAM). Heat can pose significant abiotic stress to plants and induce a rapid heat shock response, developmental alterations, chromatin decondensation, and activation of transposable elements (TEs). However, most plant heat-stress studies are conducted with seedlings, and we know very little about cell-type-specific responses. Here we use fluorescent-activated nuclear sorting to isolate and characterize stem cells of wild type and mutants defective in TE defense and chromatin compaction after heat shock and after a long recovery. Our results indicate that stem cells can suppress heat shock response pathways to maintain developmental programs. Furthermore, mutants defective in DNA methylation fail to recover efficiently from heat stress and persistently activate heat shock factors and heat-inducible TEs. Heat stress also induces DNA methylation epimutations, especially in the CHG context, and we find hundreds of DNA methylation changes three weeks after stress. Our results underline the importance of disentangling cell type-specific environmental responses for understanding plant development.
2023-09-30 | GSE223914 | GEO
Project description:Post-embryonic plant development must be coordinated in response to and with environmental feedback. Development of above-ground organs is orchestrated from stem cells in the center of the shoot apical meristem (SAM). Heat can pose significant abiotic stress to plants and induce a rapid heat shock response, developmental alterations, chromatin decondensation, and activation of transposable elements (TEs). However, most plant heat-stress studies are conducted with seedlings, and we know very little about cell-type-specific responses. Here we use fluorescent-activated nuclear sorting to isolate and characterize stem cells of wild type and mutants defective in TE defense and chromatin compaction after heat shock and after a long recovery. Our results indicate that stem cells can suppress heat shock response pathways to maintain developmental programs. Furthermore, mutants defective in DNA methylation fail to recover efficiently from heat stress and persistently activate heat shock factors and heat-inducible TEs. Heat stress also induces DNA methylation epimutations, especially in the CHG context, and we find hundreds of DNA methylation changes three weeks after stress. Our results underline the importance of disentangling cell type-specific environmental responses for understanding plant development.
2023-09-30 | GSE223850 | GEO
Project description:Flock house virus Transcriptome or Gene expression
| PRJNA248687 | ENA
Project description:Host protein folding stress responses can play important roles in RNA virus replication and evolution. Intriguingly, prior work revealed a complicated interplay between the cytosolic proteostasis stress response, controlled by its master regulator heat shock factor 1 (HSF1) and human immunodeficiency virus-1 (HIV-1). We sought to isolate HSF1 transcription factor activity from proteostasis stress and elucidate the function of HSF1 in HIV-1 lifecycle in absence of cellular stress. We used chemical genetic, stress-independent control of HSF1 activity to establish whether and how HSF1 influences HIV-1 replication. Stress-independent HSF1 induction decreased both the total quantity and infectivity of HIV-1 virions. Moreover, HIV-1 was unable to escape HSF1-mediated restriction over the course of several serial passages. These results promote continued consideration of the heat shock response as a potential target for antiviral drugs.
2022-01-30 | GSE137591 | GEO
Project description:Dynamic nuclear SUMO modifications play essential roles in orchestrating cellular responses to proteotoxic stress, DNA damageand DNA virus infections. Here, we describe the host SUMOylation response to the nuclear-replicating RNA pathogen, influenz A virus. Using quantitative proteomics to compare SUMOylation responses to various stresses (including heat-shock), we reveal that influenza A virus infection causes unique re-targeting of SUMO1 and SUMO2 to a diverse range of host proteins involved in transcription, mRNA processing, RNA quality control and DNA damage repair. This global characterization of influenza virus-triggered SUMO remodeling provides a proteomic resource to understand host nuclear SUMOylation responses to infection.
2017-03-31 | MSV000080853 | MassIVE
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