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C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies

Research output: Contribution to journalJournal article

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  • Marina Ezcurra
  • Alexandre Benedetto
  • Thanet Sornda
  • Ann F Gilliat
  • Catherine Au
  • Qifeng Zhang
  • Sophie van Schelt
  • Alexandra L Petrache
  • Hongyuan Wang
  • Yila de la Guardia
  • Shoshana Bar-Nun
  • Eleanor Tyler
  • Michael J Wakelam
  • David Gems
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<mark>Journal publication date</mark>20/08/2018
<mark>Journal</mark>Current Biology
Issue number16
Volume28
Number of pages13
Pages (from-to)2544-2556.e5
Publication statusPublished
Early online date9/08/18
Original languageEnglish

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).