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

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Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans. / Ezcurra, Marina; Benedetto, Alexandre; Sornda, Thanet et al.
In: Biorxiv, 15.12.2017.

Research output: Contribution to Journal/Magazine › Journal article

Harvard

Ezcurra, M, Benedetto, A, Sornda, T, Gilliat, A, Au, C, Zhang, Q, van Schelt, S, Petrache, AL, de la Guardia, Y, Bar-Nun, S, Tyler, E, Wakelam, MJ & Gems, D 2017, 'Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans', Biorxiv. https://doi.org/10.1101/234419

APA

Ezcurra, M., Benedetto, A., Sornda, T., Gilliat, A., Au, C., Zhang, Q., van Schelt, S., Petrache, A. L., de la Guardia, Y., Bar-Nun, S., Tyler, E., Wakelam, M. J., & Gems, D. (2017). Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans. Biorxiv. https://doi.org/10.1101/234419

Vancouver

Ezcurra M, Benedetto A, Sornda T, Gilliat A, Au C, Zhang Q et al. Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans. Biorxiv. 2017 Dec 15. doi: 10.1101/234419

Author

Ezcurra, Marina ; Benedetto, Alexandre ; Sornda, Thanet et al. / Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans. In: Biorxiv. 2017.

Bibtex

@article{88e8756f5ad946c29ee7b1489ae5fa33,
title = "Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans",
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.",
author = "Marina Ezcurra and Alexandre Benedetto and Thanet Sornda and Ann Gilliat and Catherine Au and Qifeng Zhang and {van Schelt}, Sophie and Petrache, {Alexandra L} and {de la Guardia}, Yila and Shoshana Bar-Nun and Eleonor Tyler and Wakelam, {Michael J} and David Gems",
year = "2017",
month = dec,
day = "15",
doi = "10.1101/234419",
language = "English",
journal = "Biorxiv",
publisher = "Cold Spring Harbor Laboratory Press",

}

RIS

TY - JOUR

T1 - Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans

AU - Ezcurra, Marina

AU - Benedetto, Alexandre

AU - Sornda, Thanet

AU - Gilliat, Ann

AU - Au, Catherine

AU - Zhang, Qifeng

AU - van Schelt, Sophie

AU - Petrache, Alexandra L

AU - de la Guardia, Yila

AU - Bar-Nun, Shoshana

AU - Tyler, Eleonor

AU - Wakelam, Michael J

AU - Gems, David

PY - 2017/12/15

Y1 - 2017/12/15

N2 - 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.

AB - 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.

U2 - 10.1101/234419

DO - 10.1101/234419

M3 - Journal article

JO - Biorxiv

JF - Biorxiv

ER -