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RPRD1B is required for proper heat shock response [TTchem-seq]

ABSTRACT: RPRD1B is required for proper heat shock response [TTchem-seq]

PROVIDER: PRJNA813305 | ENA |

REPOSITORIES: ENA

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RPRD1B is required for proper heat shock response [TTchem-seq]

Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In this study, we demonstrate that the RNAPII interactor RPRD1B is required for proper transcription of heat shock induced genes and for survival to heat shock.

2022-09-08 | GSE197992 | GEO

RPRD1B is required for proper heat shock response

Project description:RPRD1B is required for proper heat shock response

| PRJNA813306 | ENA

RPRD1B is required for proper heat shock response [RNA-seq]

2022-09-08 | GSE197993 | GEO

RPRD1B is required for proper heat shock response [RNA-seq]

Project description:RPRD1B is required for proper heat shock response [RNA-seq]

| PRJNA813310 | ENA

Heat shock-mediated global gene downregulation is achieved by premature transcription termination [TTchem-seq]

Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In parallel, a large portion of the genome becomes repressed. HS associated global gene repression is still largely poorly understood. In this study, we demonstrate that transcription downregulation during Heat shock is mainly achieved by premature transcription termination through the regulation of U1snRNA and the disruption of U1-telescripting.

2022-01-24 | GSE165364 | GEO

Heat shock-mediated global gene downregulation is achieved by premature transcription termination [TTchem-seq]

Project description:Heat shock-mediated global gene downregulation is achieved by premature transcription termination [TTchem-seq]

| PRJNA694162 | ENA

Nascent-protein ubiquitination is required for heat shock-induced gene downregulation in human cells.

Project description:Proteotoxic stress such as heat shock causes heat-shock factor (HSF)-dependent transcriptional upregulation of chaperones. Heat shock also leads to a rapid and reversible downregulation of many genes, a process we term stress-induced transcriptional attenuation (SITA). The mechanism underlying this conserved phenomenon is unknown. Here we report that enhanced recruitment of negative transcription elongation factors to gene promoters in human cell lines induces SITA. A chemical inhibitor screen showed that active translation and protein ubiquitination are required for the response. We further find that proteins translated during heat shock are subjected to ubiquitination and that p38 kinase signaling connects cytosolic translation with gene downregulation. Notably, brain samples of subjects with Huntington's disease also show transcriptional attenuation, which is recapitulated in cellular models of protein aggregation similar to heat shock. Thus our work identifies an HSF-independent mechanism that links nascent-protein ubiquitination to transcriptional downregulation during heat shock, with potential ramifications in neurodegenerative diseases.

2019-02-07 | GSE112379 | GEO

Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster during heat shock

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

Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

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

Caenorhabditis elegans AF4/FMR2 family homolog affl-2 regulates heat shock induced gene expression

Project description:To mitigate the deleterious effects of temperature increases on cellular organization and proteotoxicity, organisms have developed mechanisms to respond to heat stress. In eukaryotes, HSF1 is the master regulator of the heat shock transcriptional response, but the heat shock response pathway is not yet fully understood. From a forward genetic screen for suppressors of heat shock induced gene expression in Caenorhabditis elegans, we found a new allele of hsf-1 that alters its DNA-binding domain, and we found three additional alleles of sup-45, a previously molecularly uncharacterized genetic locus. We identified sup-45 as one of the two hitherto unknown C. elegans orthologs of the human AF4/FMR2 family proteins, which are involved in regulation of transcriptional elongation rate. We thus renamed sup-45 as affl-2 (AF4/FMR2-Like). Through RNA-seq, we demonstrated that affl-2 mutants are deficient in heat shock induced transcription. Additionally, affl-2 mutants have herniated intestines, while worms lacking its sole paralog (affl-1) appear wild type. AFFL-2 is a broadly expressed nuclear protein, and nuclear localization of AFFL-2 is necessary for its role in heat shock response. affl-2 and its paralog are not essential for proper HSF-1 expression and localization after heat shock, which suggests that affl-2 may function downstream or parallel of hsf-1. Our characterization of affl-2 provides insights into the regulation of heat shock induced gene expression to protect against heat stress.

2020-05-27 | GSE151164 | GEO

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