ArticleThe Journal of cell biology2023
V-ATPase/TORC1-mediated ATFS-1 translation directs mitochondrial UPR activation in C. elegans.
Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Article
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- A lysosomal surveillance response to stress extends healthspan.Nature cell biology · 2025Article
- TMBIM-2 orchestrates systemic mitochondrial stress response via facilitating Ca2+ oscillations.The Journal of cell biology · 2025Article
- SNX10 Is Involved in Ovarian Cancer Cell Metastasis by Repolarizing Tumor-Associated Macrophages Through mTOR1/Lysosomes Pathway.Biomedicines · 2025Article
- Basal Xenobot transcriptomics reveals changes and novel control modality in cells freed from organismal influence.Communications biology · 2025Article
- RAB-10 cooperates with EHBP-1 to capture vesicular carriers during post-Golgi exocytic trafficking.The Journal of cell biology · 2025Article
- V-ATPase in glioma stem cells: a novel metabolic vulnerability.Journal of experimental & clinical cancer research : CR · 2025Article
- Mitochondrial unfolded protein response in regulatory T cell function: a protective mechanism in immune aging.Frontiers in immunology · 2025Review
- Mechanisms of the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans and Mammals and Its Roles in Striated Muscles.Aging and disease · 2024Review
- A bird's eye view of mitochondrial unfolded protein response in cancer: mechanisms, progression and further applications.Cell death & disease · 2024Review
- Lysosomes mediate the mitochondrial UPR via mTORC1-dependent ATF4 phosphorylation.Cell discovery · 2023Article
- Role of UPRFrontiers in cellular and infection microbiology · 2023Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To adapt mitochondrial function to the ever-changing intra- and extracellular environment, multiple mitochondrial stress response (MSR) pathways, including the mitochondrial unfolded protein response (UPRmt), have evolved. However, how the mitochondrial stress signal is sensed and relayed to UPRmt transcription factors, such as ATFS-1 in Caenorhabditis elegans, remains largely unknown. Here, we show that a panel of vacuolar H+-ATPase (v-ATPase) subunits and the target of rapamycin complex 1 (TORC1) activity are essential for the cytosolic relay of mitochondrial stress to ATFS-1 and for the induction of the UPRmt. Mechanistically, mitochondrial stress stimulates v-ATPase/Rheb-dependent TORC1 activation, subsequently promoting ATFS-1 translation. Increased translation of ATFS-1 upon mitochondrial stress furthermore relies on a set of ribosomal components but is independent of GCN-2/PEK-1 signaling. Finally, the v-ATPase and ribosomal subunits are required for mitochondrial surveillance and mitochondrial stress-induced longevity. These results reveal a v-ATPase-TORC1-ATFS-1 signaling pathway that links mitochondrial stress to the UPRmt through intimate crosstalks between multiple organelles.
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