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

Ezcurra, Marina, Benedetto, Alexandre, Sornda, Thanet, Gilliat, Ann F., Au, Catherine, Zhang, Qifeng, van Schelt, Sophie, Petrache, Alexandra L., Wang, Hongyuan, de la Guardia, Yila, and others. (2018) C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies. Current Biology, 28 (16). pp. 2544-2556. ISSN 0960-9822. E-ISSN 1879-0445. (doi:10.1016/j.cub.2018.06.035)

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

but also of yolky lipid accumulation and redistribution (a form of senescent obesity): autophagymediated 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-toyolk 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).

Item Type: Article
DOI/Identification number: 10.1016/j.cub.2018.06.035
Uncontrolled keywords: aginga, trophy, autophagy, C. elegans, intestine, insulin/IGF-1 signaling, pathology, steatosis, vitellogenin, yolk, School of Biosciences
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: Marina Ezcurra
Date Deposited: 31 May 2019 15:00 UTC
Last Modified: 04 Feb 2020 11:37 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/74206 (The current URI for this page, for reference purposes)
Ezcurra, Marina: https://orcid.org/0000-0003-2739-6984
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