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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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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.

| S-EPMC7214782 | biostudies-literature

A delicate balance on thyroid hormones controls metabolic health and longevity in mice

Project description:A delicate balance on thyroid hormones controls metabolic health and longevity in mice

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mito-TAILS analysis of EPEC infection

Project description:Mito-TAILS N-terminomics analysis of proteolytic events during EPEC infection of human epithelial cells, on whole-cell level and mitochondria.

2020-05-21 | PXD016994 | Pride

HSF-1 promotes longevity through ubiquilin-1 dependent mitochondrial remodelling

Project description:Impaired protein homeostasis promotes age-associated tissue dysregulation, presenting a need for therapeutic approaches that can restore proteome integrity. The heat shock factor HSF-1 is the master transcriptional regulator of proteostasis and regulates the expression of heat shock proteins (HSPs), which facilitate proper protein folding, localisation, and degradation. Increased HSF-1 activity can suppress proteotoxicity and enhance longevity across species. Studies into the mechanisms behind these beneficial effects have mostly focused on HSPs; however, the precise mechanisms by which increased HSF-1 activity extends lifespan are not known. To address this, we conducted an RNAi screen for genes that promote longevity, in C. elegans over expressing HSF-1 (hsf-1 OE). We found that ubiquilin-1 (ubql-1), a multifaceted shuttle protein that functions in protein degradation pathways is necessary for full lifespan extension in hsf-1OE worms. Surprisingly, we find that lack of ubql-1 does not impact proteostasis capacity, but does alter mitochondrial dynamics, in hsf-1 OE worms. These effects are independent of mitophagy or the mitochondrial unfolded protein response (mitoUPR) suggesting enhanced turnover of mitochondrial outer membrane proteins may be important for increased longevity via the HSF-1-ubiquilin-1 axis. Additionally, we reveal a role for ubql-1, a protein quality control regulator in regulating lipid homeostasis in hsf-1 OE animals. Lack of ubql-1 in hsf-1 OE animals supresses the expression of a key mitochondrial β-oxidation and lipid mobilization gene regulated by NHR-49 - acyl-CoA synthetase-2, ACS-2 amongst other genes. We propose that ubql-1 is required for mito-fusion and metabolic modulations that promote longevity in hsf-1 OE by interacting with NHR-49.

2024-10-17 | PXD044595 | Pride

Whole-genome sequencing of Saccharomyces cerevisiae CEN.PK2-1C subjected to mtDNA base editing or Mito-BE screen

Project description:To identify mutations that occurred in the nuclear and mitochondrial DNA of the yeast subjected to mtDNA base editing or Mito-BE screen, we performed whole-genome sequencing of cultured yeast cells after isolation of mitochondrial DNA.

2024-11-01 | E-MTAB-13701 | biostudies-arrayexpress

Species comparison of liver proteomes reveals links to naked mole-rat longevity and human aging

Project description:Mammals display wide range of variation in their lifespan. Investigating the molecular networks that distinguish long- from short-lived species has proven useful to identify determinants of longevity. Here, we compared the liver of long-lived naked mole-rats (NMRs) and the phylogenetically closely related, shorter-lived, guinea pigs using an integrated omic approach. We found that NMRs livers display a unique expression pattern of mitochondrial proteins that result in distinct metabolic features of their mitochondria. For instance, we observed a generally reduced respiration rate associated with lower protein levels of respiratory chain components, particularly complex I, and increased capacity to utilize fatty acids. Interestingly, we show that the same molecular networks are affected during aging in both NMR and humans, supporting a direct link to the extraordinary longevity of both species. Finally, we identified a novel longevity pathway and validated it experimentally in the nematode C. elegans.

2018-06-21 | PXD008720 | Pride

Next Generation Sequencing of Response to Mito-Tempo in Intestinal Mucosal Biopsies from Crohn's Disease patients

Project description:Purpose: The purpose of this study was to investigate the transcriptomic changes in active Crohn's disease biopsies driven by a mitochondrial-targeted drug (Mito-Tempo)

2021-09-22 | GSE159751 | GEO

Mitochondrial Dynamics Govern Whole-body Regeneration Through Stem Cell Pluripotency and Mitonuclear Balance [scRNA-seq]

Project description:To further identity the relationship between neoblast pluripotency and mitochondrial dynamics in cell lineage commitment,single-cell RNA sequencing was used to further analyze the compositions of mito low and mito high cells

2024-11-07 | GSE244069 | GEO

CIDR Longevity Genes Project

Project description:CIDR Longevity Genes Project

| PRJNA186399 | ENA