ArticleCurrent biology : CB2018
C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies.
Article in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 115 papers.
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Who cites it
115 citing papers in PubMed, 183 citations in OpenAlex.
- Soma-to-germline miRNA inheritance through yolk promotes stress resilience in progeny.Nature structural & molecular biology · 2026Article
- Old worms, new tricks: dynamical instability explains late-life rejuvenation inbioRxiv : the preprint server for biology · 2026Article
- Strong inhibition of insulin/IGF-1 signaling in early-mid adulthood compresses morbidity, but in later life accelerates aging.bioRxiv : the preprint server for biology · 2026Article
- Autophagy: A Double-Edged Sword in the Aging ofInternational journal of molecular sciences · 2026Review
- Why we age.Biological reviews of the Cambridge Philosophical Society · 2026Review
- A conserved C. elegans zinc finger homeodomain protein, ZFH-2, is continuously required for the structural integrity and function of the alimentary tract and gonad.Development (Cambridge, England) · 2026Article
- ER remodelling is a feature of ageing and depends on ER-phagy.Nature cell biology · 2026Article
- A conservedbioRxiv : the preprint server for biology · 2026Article
- Caenorhabditis elegans as an experimental model for resilience-boosting microbiota interventions in nonmodel ectotherms.FEMS microbiology reviews · 2026Review
- Deconvolution of Single-Organism Omics Resolves Cellular and Tissue Dynamics during Aging.microPublication biology · 2026Article
- Multilayered regulation of longevity in Caenorhabditis elegans.Molecules and cells · 2026Review
- The Evolutionary Misfit: Evolution, Epigenetics, and the Rise of Non-Communicable Diseases.Epigenomes · 2025Review
- Distribution Analysis of the Lifespan Trait in Drosophila.International journal of molecular sciences · 2025Article
- RME-1-associated recycling endosomes participate in vitellogenin secretion inLife metabolism · 2025Article
- Machine learning predicts lifespan and suggests underlying causes of death in aging C. elegans.Communications biology · 2025Article
- Bacillus subtilis TO-A suppresses the age-related decline in locomotion in Caenorhabditis elegans.Communications biology · 2025Article
- Hyperactive 20Science advances · 2025Article
- The pace and shape of ant ageing.Biological reviews of the Cambridge Philosophical Society · 2025Review
- A hierarchy of causes of death in senescentbioRxiv : the preprint server for biology · 2025Article
- Condition-dependent effects of knockdown of autophagy onbioRxiv : the preprint server for biology · 2025Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
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- Erratum issued
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Aging (senescence) is characterized by the development of numerous pathologies, some of which limit lifespan. Key to understanding aging is discovery of the mechanisms (etiologies) that cause senescent pathology. In C. elegans, a major senescent pathology of unknown etiology is atrophy of its principal metabolic organ, the intestine. Here we identify a cause of not only this pathology but also of yolky lipid accumulation and redistribution (a form of senescent obesity): autophagy-mediated conversion of intestinal biomass into yolk. Inhibiting intestinal autophagy or vitellogenesis rescues both visceral pathologies and can also extend lifespan. This defines a disease syndrome leading to multimorbidity and contributing to late-life mortality. Activation of gut-to-yolk biomass conversion by insulin/IGF-1 signaling (IIS) promotes reproduction and senescence. This illustrates how major, IIS-promoted senescent pathologies in C. elegans can originate not from damage accumulation but from direct effects of futile, continued action of a wild-type biological program (vitellogenesis).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.