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Distinct cellular tools of mild hyperthermia-induced acquired stress tolerance in Chinese Hamster Ovary cells

ABSTRACT: Mild stress could help cells to survive more severe environmental or pathophysiological conditions. In the current study, we investigated the cellular mechanisms which contribute to the development of stress tolerance upon a prolonged (0-12h) fever-like (40 °C) or a moderate (42.5 °C) hyperthermia in mammalian CHO cells. Our results indicate that mild heat triggers a distinct, dose dependent remodeling of the cellular lipidome followed by the expression of heat shock proteins only at higher heat dosages. A significant elevation in the relative concentration of sat-urated membrane lipid species, specific lysophosphatidylinositol and sphingolipid species sug-gests prompt membrane microdomain reorganization and an overall membrane rigidification in response to the fluidizing heat in a time dependent manner. RNAseq experiments reveal that mild heat initiate endoplasmic reticulum stress-related signaling cascades resulting in lipid re-arrangement and ultimately in an elevated resistance against membrane fluidization by benzyl alcohol. To protect cells against lethal, protein denaturing high temperatures the classical heat shock protein response was required. The different layers of stress response elicited by different heat dosages highlights the capability of cells to utilize multiple tools to gain resistance against or to survive lethal stress conditions.

ORGANISM(S): Cricetulus griseus

PROVIDER: GSE199531 | GEO | 2022/05/18

REPOSITORIES: GEO

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Project description:The expression of heat-shock proteins (Hsps) induced by a non-lethal heat treatment confers acquired thermotolerance (AT) to organisms against a subsequent challenge of otherwise lethal temperature. After stress signal lifted, AT gradually decayed with the decline of Hsps during recovery period. The duration of AT may be critical for sessile organisms, such as plants, to survive repeated heat stress in the environment. To identify heat-induced genes involved in duration of AT, we took a reverse-genetics approach by screening for Arabidopsis T-DNA insertion mutants that show decreased thermotolerance after a long recovery at non-stress condition following a conditioning treatment. Among the tested mutants corresponding to 47 genes, only the HsfA2 knockout mutant showed significant phenotype. The mutant plants were more sensitive to severe heat stress than the wild type after long but not short recovery following a pretreatment at 37oC, which can be complemented by introducing a wild-type copy of the gene. Quantitative hypocotyl elongation assay also revealed that AT decayed faster in the absence of HsfA2. Significant decline of the transcript levels of several highly heat-induced genes was observed in the HsfA2 knockout plants after a 4-h recovery or after 2 h of prolonged heat stress. Immunoblot anlysis showed that Hsa32 and class I small Hsp were lower in the mutant than in the wild type after a long recovery. Our results suggest that HsfA2 as a heat-induced transactivator sustains the post-stress expression of Hsp genes and extends the duration of AT in Arabidopsis. Experiment Overall Design: Total RNA was isolated from the seedlings of 5-d old wild-type and HsfA2 knockout mutant seedlings (a pool of about 100 plants per treatment in duplicates) harvested immediately after heat shock treatment. In this experiment, total 12 chips were used, 1 each for 2 biological replicates of the control and HS-treated samples for the wild type and mutant plants.

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Distinct cellular tools of mild hyperthermia-induced acquired stress tolerance in Chinese Hamster Ovary cells

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