Measuring the dependence of the yeast heat shock response on intracellular pH and translation during stress
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ABSTRACT:
PROVIDER: PRJNA640923 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12062600_1.fastq.gz | Fastqsanger.gz | |||
| SRR12062600_2.fastq.gz | Fastqsanger.gz | |||
| SRR12062601_1.fastq.gz | Fastqsanger.gz | |||
| SRR12062601_2.fastq.gz | Fastqsanger.gz | |||
| SRR12062602_1.fastq.gz | Fastqsanger.gz |
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Project description:Measuring the dependence of the yeast heat shock response on intracellular pH during stress
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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.
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