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

19Citations
Citations of this article
133Readers
Mendeley users who have this article in their library.

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). Ezcurra, Benedetto et al. identify a mechanism causing aging in C. elegans: autophagy-dependent gut-to-yolk biomass conversion. This is activated by life-shortening insulin/IGF-1 signaling and causes diseases of aging, including intestinal atrophy and yolk steatosis. The mechanism involved fits the recently proposed hyper-function theory of aging.

Cite

CITATION STYLE

APA

Ezcurra, M., Benedetto, A., Sornda, T., Gilliat, A. F., Au, C., Zhang, Q., … Gems, D. (2018). C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies. Current Biology, 28(16), 2544-2556.e5. https://doi.org/10.1016/j.cub.2018.06.035

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free