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Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [MoBYSeqData]

ABSTRACT: Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [MoBYSeqData]

PROVIDER: PRJNA1120787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29306700.fastq.gz	Fastqsanger.gz
	SRR29306701.fastq.gz	Fastqsanger.gz
	SRR29306702.fastq.gz	Fastqsanger.gz
	SRR29306703.fastq.gz	Fastqsanger.gz
	SRR29306704.fastq.gz	Fastqsanger.gz

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Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [MoBYSeqData]

Project description:Premature aging is a hallmark of Down syndrome, caused by trisomy of human chromosome 21; but the reason is unclear and difficult to study in humans. We used an aneuploid model in wild yeast to show that chromosome amplification disrupts nutrient-induced cell-cycle arrest, quiescence entry, and healthy aging, across genetic backgrounds and amplified chromosomes. We discovered that these defects are due in part to aneuploidy-induced dysfunction in Ribosome Quality Control (RQC). Aneuploids entering quiescence display aberrant ribosome profiles, accumulate RQC intermediates, and harbor an increased load of protein aggregates. Although they have normal proteasome capacity, aneuploids show signs of ubiquitin dysregulation, which impacts cyclin abundance to disrupt arrest. Remarkably, inducing ribosome stalling in euploids produces similar aberrations, while up-regulating limiting RQC subunits or proteins in ubiquitin metabolism alleviates many of the aneuploid defects. Our results raise major implications for other aneuploidy disorders including Down syndrome.

2024-07-31 | GSE269237 | GEO

Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [RNASeqData]

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Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [RNASeqData]

Project description:Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [RNASeqData]

| PRJNA1120788 | ENA

Premature aging in aneuploid yeast is influenced by aneuploidy-induced defects in Ribosome Quality Control [RiboSeq]

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Premature aging in aneuploid yeast is influenced by aneuploidy-induced defects in Ribosome Quality Control [RiboSeq]

Project description:Premature aging in aneuploid yeast is influenced by aneuploidy-induced defects in Ribosome Quality Control [RiboSeq]

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Premature aging in aneuploid yeast is caused in part by aneuploidy-induced defects in Ribosome Quality Control.

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Chromosome duplication causes premature aging via defects in ribosome quality control.

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Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [HiC GGOH-treatment]

Project description:The mechanisms of aging-related oocyte aneuploidy remain elusive. Hi-C and SMART-seq revealed aging-related decreases in chromosome condensation, particularly for genomic regions proximal to the centromeres, accompanied with disrupted meiosis-associated gene expression in metaphase I (MI) aged oocytes. Further transcriptomic analysis showed that oocyte meiotic maturation was correlated with robust increases in mevalonate (MVA) pathway gene expression in young oocyte-surrounding granulosa cells (GCs), which was largely downregulated in aged GCs. Inhibtion of MVA metabolism in GCs by statins resulted in marked meiotic defects and aneuploidy in young cumulus-oocyte complexes (COCs). Conversely, supplementation with the MVA isoprenoid geranylgeraniol ameliorated meiotic defects and aneuploidy in aged COCs. Meanwhile, geranylgeraniol also activated LHR/EGF signaling in aged GCs and then enhanced the meiosis-associated gene expression in oocytes. Generally, the MVA pathway in GCs is a critical regulator of meiotic maturation and euploidy in oocytes.

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Aneuploidy-induced cellular stresses limit autophagic degradation.

Project description:An unbalanced karyotype, a condition known as aneuploidy, has a profound impact on cellular physiology and is a hallmark of cancer. Determining how aneuploidy affects cells is thus critical to understanding tumorigenesis. Here we show that aneuploidy interferes with the degradation of autophagosomes within lysosomes. Mis-folded proteins that accumulate in aneuploid cells due to aneuploidy-induced proteomic changes overwhelm the lysosome with cargo, leading to the observed lysosomal degradation defects. Importantly, aneuploid cells respond to lysosomal saturation. They activate a lysosomal stress pathway that specifically increases the expression of genes needed for autophagy-mediated protein degradation. Our results reveal lysosomal saturation as a universal feature of the aneuploid state that must be overcome during tumorigenesis.

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Aneuploidy-induced cellular stresses limit autophagic degradation.

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