Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans

Ezcurra, Marina and Benedetto, Alexandre and Sornda, Thanet and Gilliat, Ann and Au, Catherine and Zhang, Qifeng and van Schelt, Sophie and Petrache, Alexandra L and de la Guardia, Yila and Bar-Nun, Shoshana and Tyler, Eleonor and Wakelam, Michael J and Gems, David (2017) Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans. Biorxiv.

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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 Caenorhabditis 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 polymorbidity 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 continued action of a wild-type function (vitellogenesis), consistent with the recently proposed hyperfunction theory of aging.

Item Type:
Journal Article
Journal or Publication Title:
Biorxiv
ID Code:
89300
Deposited By:
Deposited On:
20 Dec 2017 09:40
Refereed?:
No
Published?:
Published
Last Modified:
16 Mar 2020 05:43