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

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

PROVIDER: PRJNA445860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6904130.fastq.gz	Fastqsanger.gz
	SRR6904140_1.fastq.gz	Fastqsanger.gz
	SRR6904140_2.fastq.gz	Fastqsanger.gz
	SRR6904150_1.fastq.gz	Fastqsanger.gz
	SRR6904150_2.fastq.gz	Fastqsanger.gz

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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

Heat shock-mediated global gene downregulation is achieved by premature transcription termination [FP_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.

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

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

2022-01-24 | GSE165364 | GEO

Heat shock-mediated global gene downregulation is achieved by premature transcription termination [4SU_mRNA-seq]

2022-01-24 | GSE165367 | GEO

Heat shock-mediated global gene downregulation is achieved by premature transcription termination

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

| PRJNA694160 | ENA

Heat Shock induces premature transcript termination and reconfigures the human transcriptome

2022-01-24 | GSE189562 | 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

Immediate transcriptional responses to heat shock of plant leaf

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.

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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

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