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Deciphering a functional gene network underlying robustness to protein overproduction

ABSTRACT: We systematically investigated the impact of genetic variation and the environment on protein overproduction costs in Saccharomyces cerevisiae To identify genes mediating protein overproduction costs, genetic perturbations were applied. The yEVenus overexpression plasmid was crossed into gene deletion backgound. The generation of double mutant strains enabled us to investigate the transcriptional response of the cells under two different internal stress: deletion of a given gene, plus the overexpression of a gratuitous protein

ORGANISM(S): Schizosaccharomyces pombe Saccharomyces cerevisiae

PROVIDER: GSE68753 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA283804

REPOSITORIES: GEO

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Deciphering a functional gene network underlying robustness to protein overproduction

Project description:We systematically investigated the impact of genetic variation and the environment on protein overproduction costs in Saccharomyces cerevisiae To identify genes mediating protein overproduction costs, genetic perturbations were applied. The yEVenus overexpression plasmid was crossed into gene deletion backgound. The generation of double mutant strains enabled us to investigate the transcriptional response of the cells under two different internal stress: deletion of a given gene, plus the overexpression of a gratuitous protein To explore the cellular response under gratuitous protein overproduction, a sensitized background was used (sse1 deletion). Our aim was to identify differentially expressed genes upon protein overproduction. 3-3 biological replicates were used for the control (single deletion strain with an empty plasmid) and for the overexpression strains (single deletion strain with yEVenus multi-copy plasmid) as well. The cellular response to overexpression was normalized to the control sse1 deletion strain, without overexpression.

2016-09-01 | E-GEOD-68753 | biostudies-arrayexpress

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Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is on the rise, and with limited pharmacological therapy available, identification of new metabolic targets is urgently needed. Oxalate is a terminal metabolite produced from glyoxylate by lactate dehydrogenase (LDHA). The liver-specific alanine-glyoxylate aminotransferase (AGXT) detoxifies glyoxylate, preventing oxalate accumulation. We report that AGXT is suppressed and LDHA is activated in livers from patients and mice with MASH, leading to oxalate overproduction. In turn, oxalate promotes steatosis in hepatocytes by inhibiting peroxisome proliferator activated receptor-alpha (PPARα) transcription and fatty acid β-oxidation (FAO), and induces monocyte chemotaxis via C-C motif chemokine ligand 2. In male mice with diet-induced MASH, blocking oxalate overproduction through hepatocyte-specific AGXT overexpression or pharmacological inhibition of LDHA potently lower steatosis, inflammation, and fibrosis by inducing PPARα-driven FAO, and suppressing monocyte chemotaxis, nuclear factor-kappaB and transforming growth factor-beta targets. These findings highlight hepatic oxalate overproduction as a new target for the treatment of MASH.

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Expression profile for overproduction of DosP

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Phosphoproteomics analysis of Pseudomonas aeruginosa with PfkA overproduction

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Expression profile for overproduction of ArT

Project description:Toxin-antitoxin (TA) systems are ubiquitous throughout bacterial and archaeal genomes. TA systems consist of a stable toxin that inhibits growth and a labile antitoxin that prevents toxicity of the toxin. Here we made an artificial TA system (arT/arA) and performed a DNA microarray study for overproduction of the toxin.

2014-05-13 | GSE54271 | GEO

Raw data for : "Genetic and pharmacological targeting of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis"

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is on the rise, and with limited pharmacological therapy available, identification of new metabolic targets is urgently needed. Oxalate is a terminal metabolite produced from glyoxylate by lactate dehydrogenase (LDHA). The liver-specific alanine-glyoxylate aminotransferase (AGXT) detoxifies glyoxylate, preventing oxalate accumulation. We report that AGXT is suppressed and LDHA is activated in livers from patients and mice with MASH, leading to oxalate overproduction. In turn, oxalate promotes steatosis in hepatocytes by inhibiting peroxisome proliferator activated receptor-alpha (PPARa) transcription and fatty acid b-oxidation (FAO), and induces monocyte chemotaxis via C-C motif chemokine ligand 2. In male mice with diet-induced MASH, blocking oxalate overproduction through hepatocyte-specific AGXT overexpression or pharmacological inhibition of LDHA potently lower steatosis, inflammation, and fibrosis by inducing PPARa-driven FAO, and suppressing monocyte chemotaxis, nuclear factor-kappa B and transforming growth factor-beta targets. These findings highlight hepatic oxalate overproduction as a new target for the treatment of MASH.

2024-04-21 | MSV000094587 | MassIVE

Expression profile for overproduction of ArT

2014-05-13 | E-GEOD-54271 | biostudies-arrayexpress

Genetic and pharmacological targeting of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis

Project description:Genetic and pharmacological targeting of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis

| PRJNA1105091 | ENA

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