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RNA-seq data for: A conserved mito-cytoplasmic translational balance links two longevity pathways

ABSTRACT: Slowing down mRNA translation in either the cytoplasm or the mitochondria are both conserved longevity mechanisms. Here, we found a non-interventional natural correlation of mitochondrial and cytoplasmic ribosomal proteins when looking at mouse population genetics, suggesting a mito-cytoplasmic translational balance. Additionally, inhibiting mitochondrial translation in C. elegans in turn reduced cytoplasmic translation and repressed growth pathways while upregulating stress responses at both proteome and transcriptome levels. This coordinated repression of cytoplasmic translation is dependent on the atf-5/Atf4 transcription factor and is conserved in mammalian cells upon inhibiting mitochondrial translation pharmacologically with the antibiotic doxycycline. Lastly, extending this to a mammalian setting using doxycycline-treated germ-free mice, we found repressed cytoplasmic translation and ribosomal proteins in liver. These data demonstrate that inhibiting mitochondrial translation initiates a signaling cascade leading to coordinated repression of cytoplasmic translation, unlike previously described unidirectional cyto-to-mito translational communication in yeast, which can be targeted to promote healthy aging.

ORGANISM(S): Mus musculus Caenorhabditis elegans

PROVIDER: GSE122097 | GEO | 2019/12/11

REPOSITORIES: GEO

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The ribosomal protein Asc1/RACK1 is required for efficient translation of short mRNAs

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MicroRNA Directly Enhances Mitochondrial Translation during Muscle Differentiation.

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Protein Kinase A Regulates Gene-Specific Translational Adaptation in Differentiating Yeast

Project description:Cellular differentiation is driven by coordinately regulated changes in gene expression. Translational control of gene expression is increasingly recognized as pervasive and quantitatively significant, but the mechanisms responsible for widespread changes in gene-specific translation activity are largely unknown. Here we investigate the mechanisms responsible for translational reprogramming during cellular adaptation to the absence of glucose, a stimulus that induces invasive filamentous differentiation in yeast. We show that gene-specific translation efficiencies are highly adapted to cellular conditions and that glucose withdrawal is accompanied by widespread translational reprogramming at the level of translation initiation. We demonstrate that transcripts from <5% of genes make up the majority of translating mRNA in both rapidly dividing and starved cells. Moreover, the identities of these highly translated genes are growth-state specific, and they are subject to condition-dependent translational privilege. By comparing glucose starvation to other growth-attenuating stresses, we distinguish a glucose-specific translational response that regulates ribosomal protein and mitochondrial protein-coding genes. This response is mediated through signaling by protein kinase A (PKA). These findings reveal a high degree of growth-state specialization of the translatome and identify PKA as an important regulator of gene-specific translation activity. Examine translational adaptation in yeast in response to glucose starvation

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RNA-seq data for: A conserved mito-cytoplasmic translational balance links two longevity pathways

Project description:RNA-seq data for: A conserved mito-cytoplasmic translational balance links two longevity pathways

| PRJNA503572 | ENA

A genome-scale analysis of mitochondrial-associated mRNAs in plants: upstream AUGs in 5’UTRs alter mRNA targeting

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Transcription profiling of Arabidopsis eif3h mutants vs. wild type

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