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

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C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies. / Ezcurra, Marina; Benedetto, Alexandre; Sornda, Thanet et al.
In: Current Biology, Vol. 28, No. 16, 20.08.2018, p. 2544-2556.e5.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Ezcurra, M, Benedetto, A, Sornda, T, Gilliat, AF, Au, C, Zhang, Q, van Schelt, S, Petrache, AL, Wang, H, de la Guardia, Y, Bar-Nun, S, Tyler, E, Wakelam, MJ & Gems, D 2018, 'C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies', Current Biology, vol. 28, no. 16, pp. 2544-2556.e5. https://doi.org/10.1016/j.cub.2018.06.035

APA

Ezcurra, M., Benedetto, A., Sornda, T., Gilliat, A. F., Au, C., Zhang, Q., van Schelt, S., Petrache, A. L., Wang, H., de la Guardia, Y., Bar-Nun, S., Tyler, E., Wakelam, M. J., & 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

Vancouver

Ezcurra M, Benedetto A, Sornda T, Gilliat AF, Au C, Zhang Q et al. C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies. Current Biology. 2018 Aug 20;28(16):2544-2556.e5. Epub 2018 Aug 9. doi: 10.1016/j.cub.2018.06.035

Author

Ezcurra, Marina ; Benedetto, Alexandre ; Sornda, Thanet et al. / C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies. In: Current Biology. 2018 ; Vol. 28, No. 16. pp. 2544-2556.e5.

Bibtex

@article{c7a05ba15a34443dacb3ad1558eab16b,
title = "C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies",
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).",
keywords = "Journal Article",
author = "Marina Ezcurra and Alexandre Benedetto and Thanet Sornda and Gilliat, {Ann F} and Catherine Au and Qifeng Zhang and {van Schelt}, Sophie and Petrache, {Alexandra L} and Hongyuan Wang and {de la Guardia}, Yila and Shoshana Bar-Nun and Eleanor Tyler and Wakelam, {Michael J} and David Gems",
note = "Copyright {\textcopyright} 2018 The Author(s). Published by Elsevier Ltd.. All rights reserved.",
year = "2018",
month = aug,
day = "20",
doi = "10.1016/j.cub.2018.06.035",
language = "English",
volume = "28",
pages = "2544--2556.e5",
journal = "Current Biology",
issn = "0960-9822",
publisher = "CELL PRESS",
number = "16",

}

RIS

TY - JOUR

T1 - C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies

AU - Ezcurra, Marina

AU - Benedetto, Alexandre

AU - Sornda, Thanet

AU - Gilliat, Ann F

AU - Au, Catherine

AU - Zhang, Qifeng

AU - van Schelt, Sophie

AU - Petrache, Alexandra L

AU - Wang, Hongyuan

AU - de la Guardia, Yila

AU - Bar-Nun, Shoshana

AU - Tyler, Eleanor

AU - Wakelam, Michael J

AU - Gems, David

N1 - Copyright © 2018 The Author(s). Published by Elsevier Ltd.. All rights reserved.

PY - 2018/8/20

Y1 - 2018/8/20

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 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).

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 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).

KW - Journal Article

U2 - 10.1016/j.cub.2018.06.035

DO - 10.1016/j.cub.2018.06.035

M3 - Journal article

C2 - 30100339

VL - 28

SP - 2544-2556.e5

JO - Current Biology

JF - Current Biology

SN - 0960-9822

IS - 16

ER -