Measuring the dependence of the yeast heat shock response on intracellular pH and translation during stress
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PROVIDER: PRJNA640923 | ENA |
REPOSITORIES: ENA
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Project description:Measuring the dependence of the yeast heat shock response on intracellular pH during stress
| PRJNA599929 | ENA
Project description:S. cerevisiae cells acidify when they experience stressful temperatures. To determine whether this heat-shock associated acidification is important for the cellular response, we manipulated intracellular pH, heat shocked cells, and sequenced the transcriptome.
2020-06-30 | GSE143292 | GEO
Project description:S. cerevisiae cells acidify when they experience stressful temperatures. In addition, newly-translated proteins are thought to misfold, triggering the heat shock response. To determine whether heat-shock associated acidification and translation state are important for the cellular response, we manipulated intracellular pH, blocked translation, heat shocked cells, and sequenced the transcriptome.
2020-06-30 | GSE152916 | GEO
Project description:Hepatitis B virus (HBV) contains a partially double-stranded relaxed circular DNA (rcDNA) genome that is converted into a covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocyte by cellular DNA repair machinery. cccDNA associates with nucleosomes to form a minichromosome that transcribes RNA to support the expression of viral proteins and reverse transcriptional replication of viral DNA. In addition to the de novo synthesis from incoming virion rcDNA, cccDNA can also been synthesized from rcDNA in the progeny nucleocapsids in the cytoplasm of infected hepatocytes via the intracellular amplification pathway. In our efforts to identify cellular DNA repair proteins required for cccDNA synthesis by a chemogenetic screen, we found that B02, a small molecular inhibitor of DNA homologous recombination repair protein RAD51, significantly enhanced the synthesis of cccDNA via intracellular amplification pathway in human hepatoma cells. Ironically, neither siRNA knockdown of RAD51 expression nor treatment with another structurally distinct RAD51 inhibitor or activator altered cccDNA amplification. However, further mechanistic studies revealed that B02 treatment significantly elevated the levels of multiple heat shock protein mRNA and siRNA knockdown of HSPA1A expression or treatment with HSPA1 inhibitors significantly attenuated B02 enhancement of cccDNA amplification. Moreover, B02 enhanced cccDNA amplification was efficiently inhibited by compounds that selectively inhibit DNA polymerase α or topoisomerase II, the enzymes required for cccDNA intracellular amplification. Our results thus indicate that B02 treatment induces a heat shock protein-mediated cellular response that positively regulates the conversion of rcDNA into cccDNA via the authentic intracellular amplification pathway
2022-12-08 | GSE209863 | GEO
Project description:Amongst several amoebic species that colonize the human gut only Entamoeba histolytica is able to cause tissue damage in the intestine and other organs. Amoebic pathogenicity and virulence are commonly evaluated as the parasiteM-+s ability to produce liver abscesses in hamsters (ALAH). Some molecules involved in several functions that enable E. histolytica to invade and survive in the tissues have been identified and proposed as virulence factors. However, despite the fact that during early tissue invasion E. histolytica has to cope with toxic oxygen concentrations, little attention have received the mechanisms of oxygen resistance and its relationship with pathogenicity and virulence. In this work we compared the ability of virulent E. histolytica, non virulent E. histolytica and non pathogenic E. dispar to survive under physiological oxygen concentrations. Also, the effect of hyperoxia on the transcriptome, the oxygen reduction pathway, iron-sulfur protein oxidation, protein carbonylation and complement resistance was analyzed. Our results showed that a low oxygen reduction capacity plus high complement susceptibility contribute to the inability of E. dispar to survive during the early tissue invasion. On the other hand, under hyperoxia, the non virulent E. histolytica phenotype was associated with a defect in the up-regulation of genes of the heat-shock response which correlated with accumulation of oxidized proteins and irreversible PFOR inactivation. We conclude that maintenance of an intracellular hypoxic environment and up regulation of the heat-shock protein response for proper metabolic functioning are primary requirements for amoebic pathogenicity and virulence.
2015-03-02 | E-MTAB-1207 | biostudies-arrayexpress
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:Cells adapt to environmental stressors such as heat shock and extracellular acidosis through formation of nuclear membrane-less compartments called Amyloid bodies (A-bodies). Stressors activate formation of Amyloid bodies (A-bodies) via induction of ribosomal intergenic spacer RNA (rIGSRNA). RNA-seq on non-ribosome depleted RNA from human MCF7 cells exposed to heat shock (43C, 30 minutes) revealed the heat shock-specific expression profile of rIGSRNA.
2018-08-02 | GSE115731 | GEO
Project description:Entamoeba histolytica is a protozoan parasite which causes colitis and liver abscesses. A pilot microarray consisting of 360 unique parasite genes was constructed using identical methods to the larger array (1,971 unique genes). The four arrays in this data set were used to ascertain whether the microarrays would be useful in detecting changes in transcript abundance by exposing parasites to heat shock (42 0C for 1 hr). Approximately, 17% of the genes were regulated by at least two fold including many genes previously shown to be involved in heat shock response. This data confirmed that the genomic DNA arrays were useful in detecting changes in transcript abundance. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-07-22 | GSE2978 | 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