ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2019
Production of YP170 Vitellogenins Promotes Intestinal Senescence in Caenorhabditis elegans.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Soma-to-germline miRNA inheritance through yolk promotes stress resilience in progeny.Nature structural & molecular biology · 2026Article
- 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
- 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
- Preconception exposure to perfluorooctanesulfonic acid (PFOS) and perfluorobutanesulfonic acid (PFBS) impaired reproduction via insulin/insulin-like growth factor signaling pathway without effects on the second generation inToxicology reports · 2025Article
- SRS microscopy identifies inhibition of vitellogenesis as a mediator of lifespan extension by caloric restriction inbioRxiv : the preprint server for biology · 2025Article
- Loss of the vitellogenins confers a fitness disadvantage but does not impact brood size inmicroPublication biology · 2025Article
- Caffeine-Induced Upregulation ofNutrients · 2024Article
- Decoding lifespan secrets: the role of the gonad inFrontiers in aging · 2024Review
- C. elegans ageing is accelerated by a self-destructive reproductive programme.Nature communications · 2023Article
- Yolk-deprivedLife science alliance · 2023Article
- Modalities of aging in organisms with different strategies of resource allocation.Ageing research reviews · 2022Review
- Fusion and expansion of vitellogenin vesicles during Caenorhabditis elegans intestinal senescence.Aging cell · 2022Article
- Gonadotropin-releasing hormone-like receptor 2 inversely regulates somatic proteostasis and reproduction inFrontiers in cell and developmental biology · 2022Article
- Semelparous Death as one Element of Iteroparous Aging Gone Large.Frontiers in genetics · 2022Article
- C. elegans feed yolk to their young in a form of primitive lactation.Nature communications · 2021Article
- The Mitochondrial Prohibitin (PHB) Complex inMetabolites · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During aging, etiologies of senescence cause multiple pathologies, leading to morbidity and death. To understand aging requires identification of these etiologies. For example, Caenorhabditis elegans hermaphrodites consume their own intestinal biomass to support yolk production, which in later life drives intestinal atrophy and ectopic yolk deposition. Yolk proteins (YPs; vitellogenins) exist as three abundant species: YP170, derived from vit-1-vit-5; and YP115 and YP88, derived from vit-6. Here, we show that inhibiting YP170 synthesis leads to a reciprocal increase in YP115/YP88 levels and vice versa, an effect involving posttranscriptional mechanisms. Inhibiting YP170 production alone, despite increasing YP115/YP88 synthesis, reduces intestinal atrophy as much as inhibition of all YP synthesis, which increases life span. By contrast, inhibiting YP115/YP88 production alone accelerates intestinal atrophy and reduces life span, an effect that is dependent on increased YP170 production. Thus, despite copious abundance of both YP170 and YP115/YP88, only YP170 production is coupled to intestinal atrophy and shortened life span. In addition, increasing levels of YP115/YP88 but not of YP170 increases resistance to oxidative stress; thus, longevity resulting from reduced vitellogenin synthesis is not attributable to oxidative stress resistance.
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