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Not1 and Not4 inversely determine mRNA solubility that sets the dynamics of co-translational events

ABSTRACT: The goal is to compare role of Not1,4,5 in co-translational decay and solubility of RNAs from soluble and total RNA pools using degron strains

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE193912 | GEO | 2023/01/24

REPOSITORIES: GEO

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Not1 and Not4 inversely determine mRNA solubility that sets the dynamics of co-translational events

Project description:Comparison of overall tRNA level and fraction of charged tRNAs upon treatment with auxin to deplete Not1 in the degron strain and compared to untreated cells.

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Not1 and Not4 inversely determine mRNA solubility that sets the dynamics of co-translational events.

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Not1 and Not4 inversely determine mRNA solubility that sets the dynamics of co-translational events

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Not1 and Not4 inversely determine mRNA solubility that sets the dynamics of co-translational events

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Co-translational regulation of Mmf1 expression depends upon its mitochondrial targeting, ubiquitination of Egd1 by Not4, Caf130 and NGD: MitoENCay

Project description:The Ccr4-Not complex is a conserved multi protein complex with diverse roles in the mRNA life cycle. Recently we determined that the Not1 and Not4 subunits of Ccr4-Not inversely regulate mRNA solubility and thereby impact dynamics of co-translation events. One mRNA whose solubility is most extremely inversely regulated by Not1 and Not4 is MMF1 encoding a mitochondrial protein that is translated with apparent ribosome pausing. In this work we uncover a mechanism that limits MMF1 overexpression in fermenting yeast and does not require MMF1 5’ or 3’ untranslated sequences but is mediated solely by the MMF1 coding sequence. This mechanism depends upon co-translational targeting of the MMF1 mRNA to the mitochondria, promoted by its mitochondrial targeting sequence, the Egd1 subunit of the NAC complex, the Om14 outer membrane protein and components of the mitochondrial import machinery as well as by Not4. Thereby, levels and translation of the MMF1 mRNA are limited by a mechanism that we have named Mito-ENCay involving ubiquitination of Egd1 by Not4, the Caf130 subunit of the Ccr4-Not complex and RQC. Our results indicate that this mechanism is used for highly expressed mRNAs that depend upon co-translational interactions for appropriate folding, such as ribosomal protein mRNAs in fermenting yeast.

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Project description:Cells maintain metabolite homeostasis (metabolostasis) by buffering fluctuations in metabolite levels, yet the limits of this buffering and the mechanisms underlying metabolic toxicity remain poorly understood. To study this, we systematically overfed metabolites in Saccharomyces cerevisiae and quantified associations with growth inhibition, intracellular aggregation, and multiomic perturbations. We identify metabolite-specific failure thresholds at which amyloid-like aggregates are observed, with graded growth inhibition detectable at sub-threshold concentrations, suggesting toxicity mechanisms beyond transporter saturation. Metabolites with higher network influence and broader pathway participation are associated with higher failure thresholds and smaller pathway disturbances. These patterns are associated with chemical properties and solubility: more soluble metabolites, while broadly tolerated, are associated with localised aggregates at their failure thresholds, whereas less soluble metabolites are associated with larger systemic pathway disruptions. Multiomic integration identifies a two-tiered translational regulatory architecture characterising cellular resilience to metabolic overfeeding. General resilience is associated with transcriptional commitment to resource conservation via attenuation of anabolic pathways. Metabolite-specific defense is characterised by high-magnitude translational regulatory events; for example, engagement of aromatic catabolism under phenylalanine overfeeding and energetic control pathways under glycine overfeeding. Together, our results operationally define metabolostasis as a cellular system associated with constraint of metabolite concentrations, coordination of network and pathway-level regulation, and buffering against amyloid-like aggregation, highlighting how network topology, pathway architecture, and chemical properties are associated with metabolic resilience and toxicity thresholds.

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