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Aneuploidy-induced proteotoxic stress can be effectively tolerated without dosage compensation, genetic mutations or stress responses

ABSTRACT: Aneuploidy-induced proteotoxic stress can be effectively tolerated without dosage compensation, genetic mutations or stress responses

PROVIDER: PRJNA590714 | ENA |

REPOSITORIES: ENA

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Aneuploidy-induced proteotoxic stress can be effectively tolerated without dosage compensation, genetic mutations or stress responses

Project description:The protein homeostasis (proteostasis) network maintains balanced protein synthesis, folding, transport and degradation within a cell. Because failure to maintain proteostasis is associated with aging and disease, a concerted effort has been placed on studying how the proteostasis network responds to various stresses. Typically, this is accomplished using ectopic overexpression of well-characterized, model misfolded protein substrates; however, how cells tolerate large-scale, diverse burden to the proteostasis network is not understood. Aneuploidy, the state of imbalanced chromosome content, adversely affects the proteostasis network by dysregulating the expression of hundreds of proteins simultaneously. Using aneuploid yeast cells as a model, we address what compensatory adjustments enable cells to tolerate large-scale, diverse challenges to the proteostasis network. Here we show adapted aneuploid Saccharomyces cerevisiae strains that exhibit robust growth and enhanced stress tolerance associated with enhancement of translation, folding, and quality control systems without genetic changes or activation of canonical stress response pathways.

2020-08-17 | GSE140733 | GEO

Aneuploidy-induced proteotoxic stress can be effectively tolerated without dosage compensation, genetic mutations, or stress responses.

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The deregulated microRNAome contributes to the cellular response to aneuploidy [miRNA]

Project description:Aneuploidy severely alters cell physiology and is widespread in cancers and other pathologies. In model cell lines, aneuploidy impairs proliferation, leads to proteotoxic as well as replication stress and triggers conserved transcriptome and proteome changes. In this study we analysed for the first time miRNAs and demonstrate that their expression is altered in response to chromosome gain.

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The deregulated microRNAome contributes to the cellular response to aneuploidy [mRNA]

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RNA-seq: WT under proteotoxic stress conditions

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The integrated stress response protects microtubule dynamics to recover from proteotoxic stress

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Proteotoxic stress-induced apoptosis in cancer cells: understanding the susceptibility and enhancing the potency

Project description:Leiomyosarcoma (LMS) is an aggressive cancer with few therapeutic options. LMS cells are more sensitive to proteotoxic stress compared to normal smooth muscle cells. We used small compound 2c to induce proteotoxic stress and compare the transcriptomic adaptations of immortalized human uterine smooth muscle cells (HUtSMC) and LMS cells SK-UT-1. We found that the expression of the heat shock proteins (HSP) gene family is upregulated with higher efficiency in normal cells. In contrast, upregulation of BH3-only proteins is higher in LMS cells. HSF1, the master regulator of HSP transcription, is sequestered into transcriptionally incompetent nuclear foci only in LMS cells, which explains the lower HSP upregulation. We also found that several compounds can enhance the cell death response to proteotoxic stress. Specifically, when low doses were used, an inhibitor of salt-inducible kinases (SIKs) and the inhibitor of IRE1, a key element of the unfolded protein response (UPR), support proteotoxic-induced cell death with strength in LMS cells and without effects on the survival of normal cells. Overall, our data provide an explanation for the higher susceptibility of LMS cells to proteotoxic stress and suggest a potential option for co-treatment strategies.

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2023-09-27 | GSE224992 | GEO

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