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

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

PROVIDER: PRJNA503572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8146680_1.fastq.gz	Fastqsanger.gz
	SRR8146680_2.fastq.gz	Fastqsanger.gz
	SRR8146690_1.fastq.gz	Fastqsanger.gz
	SRR8146690_2.fastq.gz	Fastqsanger.gz
	SRR8146700_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2019-12-11 | GSE122097 | GEO

A Conserved Mito-Cytosolic Translational Balance Links Two Longevity Pathways.

Project description:Slowing down translation in either the cytosol or the mitochondria is a conserved longevity mechanism. Here, we found a non-interventional natural correlation of mitochondrial and cytosolic ribosomal proteins (RPs) in mouse population genetics, suggesting a translational balance. Inhibiting mitochondrial translation in C. elegans through mrps-5 RNAi repressed cytosolic translation. Transcriptomics integrated with proteomics revealed that this inhibition specifically reduced translational efficiency of mRNAs required in growth pathways while increasing stress response mRNAs. The repression of cytosolic translation and extension of lifespan from mrps-5 RNAi were dependent on atf-5/ATF4 and independent from metabolic phenotypes. We found the translational balance to be conserved in mammalian cells upon inhibiting mitochondrial translation pharmacologically with doxycycline. Lastly, extending this in vivo, doxycycline repressed cytosolic translation in the livers of germ-free mice. These data demonstrate that inhibiting mitochondrial translation initiates an atf-5/ATF4-dependent cascade leading to coordinated repression of cytosolic translation, which could be targeted to promote longevity.

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