ArticleProceedings of the National Academy of Sciences of the United States of America2014
Dynamic JUNQ inclusion bodies are asymmetrically inherited in mammalian cell lines through the asymmetric partitioning of vimentin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Proteostasis and ageing dissidence.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- A designed ubiquitin-binding protein selectively enriches and visualizes unanchored ubiquitin.Science advances · 2026Article
- The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer.Molecular oncology · 2026Review
- Stress-induced nucleolar rejuvenation via chaperone-mediated segregation in a filamentous fungus.The Journal of cell biology · 2026Article
- Gene expression and co-expression heterogeneity patterns and biodemography analyses during the cell cycle encourage aging studies in archaea.GeroScience · 2026Article
- Silent forces, hidden currents: the influence of static magnetic field stimulation on tumor biophysics.npj biomedical innovations · 2026Review
- Cell membrane asymmetries and cellular aging.The Biochemical journal · 2025Review
- Maturation and detoxification of synphilin-1 inclusion bodies regulated by sphingolipids.eLife · 2025Article
- The Ile35 Residue of the ALS-Associated Mutant SOD1 Plays a Crucial Role in the Intracellular Aggregation of the Molecule.Molecular neurobiology · 2025Article
- Unveiling Lipid Droplet Transport Dynamics as Biomarkers of Senescence Using Label-Free, Time-Lapse Holotomography.Aging and disease · 2025Article
- iPAR: a new reporter for eukaryotic cytoplasmic protein aggregation.BMC methods · 2025Article
- TDP43 aggregation at ER-exit sites impairs ER-to-Golgi transport.Nature communications · 2024Article
- Using deep learning to decipher the impact of telomerase promoter mutations on the dynamic metastatic morpholome.PLoS computational biology · 2024Article
- K29-linked free polyubiquitin chains affect ribosome biogenesis and direct ribosomal proteins to the intranuclear quality control compartment.Molecular cell · 2024Article
- Sequestrase chaperones protect against oxidative stress-induced protein aggregation and [PSI+] prion formation.PLoS genetics · 2024Article
- Characterization of Spatial Differences in Two Misfolded Proteins During Aggresome Formation.microPublication biology · 2024Article
- Sialoadhesin-dependent susceptibility and replication of porcine reproductive and respiratory syndrome viruses in CD163-expressing cells.Frontiers in veterinary science · 2024Article
- Metabolic and proteostatic differences in quiescent and active neural stem cells.Neural regeneration research · 2024Review
- Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is associated with the accumulation of several types of damage: in particular, damage to the proteome. Recent work points to a conserved replicative rejuvenation mechanism that works by preventing the inheritance of damaged and misfolded proteins by specific cells during division. Asymmetric inheritance of misfolded and aggregated proteins has been shown in bacteria and yeast, but relatively little evidence exists for a similar mechanism in mammalian cells. Here, we demonstrate, using long-term 4D imaging, that the vimentin intermediate filament establishes mitotic polarity in mammalian cell lines and mediates the asymmetric partitioning of damaged proteins. We show that mammalian JUNQ inclusion bodies containing soluble misfolded proteins are inherited asymmetrically, similarly to JUNQ quality-control inclusions observed in yeast. Mammalian IPOD-like inclusion bodies, meanwhile, are not always inherited by the same cell as the JUNQ. Our study suggests that the mammalian cytoskeleton and intermediate filaments provide the physical scaffold for asymmetric inheritance of dynamic quality-control JUNQ inclusions. Mammalian IPOD inclusions containing amyloidogenic proteins are not partitioned as effectively during mitosis as their counterparts in yeast. These findings provide a valuable mechanistic basis for studying the process of asymmetric inheritance in mammalian cells, including cells potentially undergoing polar divisions, such as differentiating stem cells and cancer cells.
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