Cell Specific Transcriptional Responses to Heat Shock in the Mouse Utricle Epithelium
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PROVIDER: PRJNA580444 | ENA |
REPOSITORIES: ENA
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Project description:To determine the transcriptional responses to heat shock of inner ear sensory hair cells and supporting cells, we performed cell-type-specific transcriptional profiling using the RiboTag method, which allows for immunoprecipitation of actively translating mRNAs from specific cell types. RNA-Seq differential gene expression analyses demonstrated that RiboTag identified known cell type-specific markers as well as new markers for hair cells and supporting cells. Gene expression differences suggest that both hair cells and supporting cells exhibit a transcriptional heat shock response. However, hair cells and supporting cells expressed different members of the heat shock protein family in response to heat stress, and supporting cells expressed a larger number of HSPs. Only one HSP, Chaperonin Containing T-Complex Polypeptide 1 Subunit 8, (CCT8) was uniquely induced in hair cells. Together our data indicate that hair cells exhibit a limited but unique heat shock response, and supporting cells exhibit a broader and more robust transcriptional response to protective heat stress.
2020-05-05 | GSE139593 | GEO
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Project description:The vestibular sensory epithelium may degenerate into a layer of flat cells, known as flat epithelium, after a severe lesion, but the pathogenesis of vestibular flat epithelium remains unclear. We used microarrays to detail the global programme of gene expression in normal utricle and vestibular flat epithelium and identified whether epithelial-mesenchymal transition participite in this process
2021-09-30 | GSE179063 | GEO
Project description:Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster. Heat shock factor IP DNA or Mock IP DNA from heat shocked Kc 167 cells compared to whole cell extract on Agilent 2x244k tiling arrays.
2011-01-05 | GSE19744 | GEO
Project description:Recombinant Escherichia coli cultures are used to manufacture numerous therapeutic proteins and industrial enzymes, where many of these processes use elevated temperatures to induce recombinant protein production. The heat-shock response in wild-type E. coli has been well studied. In this study, the transcriptome profiles of recombinant E. coli subjected to a heat-shock and to a dual heat-shock recombinant protein induction were examined. Most classical heat-shock protein genes were identified as regulated in both conditions. The major transcriptome differences between the recombinant and reported wild-type cultures were heavily populated by hypothetical and putative genes, which indicates recombinant cultures utilize many unique genes to respond to a heat-shock. Comparison of the dual stressed culture data with literature recombinant protein induced culture data revealed numerous differences. The dual stressed response encompassed three major response patterns: induced-like, in-between, and greater than either individual stress response. Also, there were no genes that only responded to the dual stress. The most interesting difference between the dual stressed and induced cultures was the amino acid-tRNA gene levels. The amino acid-tRNA genes were elevated for the dual cultures compared to the induced cultures. Since tRNAs facilitate protein synthesis via translation, this observed increase in amino acid-tRNA transcriptome levels, in concert with elevated heat-shock chaperones, might account for improved productivities often observed for thermo-inducible systems. Most importantly, the response of the recombinant cultures to a heat-shock was more profound than wild-type cultures, and further, the response to recombinant protein induction was not a simple additive response of the individual stresses. The objective of the present work is to gain a better understanding of the heat-shock response in recombinant cultures and how this response might impact recombinant protein production. To accomplish this objective, the transcriptome response of recombinant cultures subjected to a heat-shock and a dual heat-shock recombinant protein induction were analyzed. The transcriptome levels were determined using Affymetrix E. coli Antisense DNA microarrays, such that the entire genome was evaluated. These two transcriptome responses were also compared to recombinant cultures at normal growth temperature that were not over-expressing the recombinant protein and a set of literature recombinant culture data that were chemically induced to over-express the recombinant protein. Additionally, the heat-shock response of the recombinant cultures was compared to the literature report of the heat-shock response in wild-type cultures. The results of the global transcriptome analysis demonstrated that recombinant cultures respond differently to a heat-shock stress than wild-type cultures, where the transcriptome response of the recombinant cultures is further modified by production of a recombinant protein.
2009-08-07 | GSE17507 | GEO
Project description:Ambient temperature is one of the most important environment factors that direct all organisms for morphogenesis, metabolisms and growth. Plants have evolved efficient mechanisms adapting temperature fluctuation such as heat stress response (HSR). Although transcriptional regulatory network of plant HSR has been established, little is known on the genome-wide transcriptional changes within first several minutes upon heat shock (HS). To precisely measure the very first wave of transcriptional response to HS, we investigated the nascent RNA and mature mRNA from plant leaf tissue exposure to 5-min HS treatment using global run-on sequencing (GRO-seq) and RNA sequencing (RNA-seq) methods. We found that only a small group of genes were both up- or down-regulated at nascent RNA and mRNA levels. Primed plants that already exposed to a mild heat stress induced a more drastic transcriptomic alteration than naïve plants which had not experienced a heat stress. Group A1 HEAT SHOCK TRANSCRIPTION FACTORs (HsfA1s) are the major transcription factors in charge of the very early transcriptional HSR. Within 5-minute HS, we also observed that: 1) Engaged RNA polymerase II (Pol II) was accumulated downstream of transcription start sites; 2) 5' pause-release is a rate limiting step for induction of some heat shock protein genes; 3) A good number of genes switched transcription modes; 4) Pervasive read-through was induced at terminators. Plants' HSR is transcriptionally very quick. GRO-seq is sensitive and robust to detect quick response to HS. Heat stress memory takes place at multiple steps of transcription cycles such as Pol II recruitment, 5' pausing, elongation and termination.
2020-07-11 | GSE128698 | GEO
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules).
2011-11-09 | GSE24197 | GEO
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