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The role of autophagy during the early neonatal starvation period

Author

Listed:
  • Akiko Kuma

    (Japan Science and Technology Agency
    Chiba University
    National Institute for Basic Biology, he Graduate University for Advanced Studies
    Tokyo Metropolitan Institute of Medical Science)

  • Masahiko Hatano

    (Chiba University
    Chiba University)

  • Makoto Matsui

    (National Institute for Basic Biology, he Graduate University for Advanced Studies
    School of Life Science, the Graduate University for Advanced Studies
    Tokyo Metropolitan Institute of Medical Science)

  • Akitsugu Yamamoto

    (Nagahama Institute of Bio-Science and Technology)

  • Haruaki Nakaya

    (Chiba University Graduate School of Medicine, Chiba University)

  • Tamotsu Yoshimori

    (National Institute of Genetics)

  • Yoshinori Ohsumi

    (National Institute for Basic Biology, he Graduate University for Advanced Studies
    School of Life Science, the Graduate University for Advanced Studies)

  • Takeshi Tokuhisa

    (Chiba University)

  • Noboru Mizushima

    (Japan Science and Technology Agency
    National Institute for Basic Biology, he Graduate University for Advanced Studies
    Tokyo Metropolitan Institute of Medical Science)

Abstract

At birth the trans-placental nutrient supply is suddenly interrupted, and neonates face severe starvation until supply can be restored through milk nutrients1. Here, we show that neonates adapt to this adverse circumstance by inducing autophagy. Autophagy is the primary means for the degradation of cytoplasmic constituents within lysosomes2,3,4. The level of autophagy in mice remains low during embryogenesis; however, autophagy is immediately upregulated in various tissues after birth and is maintained at high levels for 3–12 h before returning to basal levels within 1–2 days. Mice deficient for Atg5, which is essential for autophagosome formation, appear almost normal at birth but die within 1 day of delivery. The survival time of starved Atg5-deficient neonates (∼ 12 h) is much shorter than that of wild-type mice (∼ 21 h) but can be prolonged by forced milk feeding. Atg5-deficient neonates exhibit reduced amino acid concentrations in plasma and tissues, and display signs of energy depletion. These results suggest that the production of amino acids by autophagic degradation of ‘self’ proteins, which allows for the maintenance of energy homeostasis, is important for survival during neonatal starvation.

Suggested Citation

  • Akiko Kuma & Masahiko Hatano & Makoto Matsui & Akitsugu Yamamoto & Haruaki Nakaya & Tamotsu Yoshimori & Yoshinori Ohsumi & Takeshi Tokuhisa & Noboru Mizushima, 2004. "The role of autophagy during the early neonatal starvation period," Nature, Nature, vol. 432(7020), pages 1032-1036, December.
  • Handle: RePEc:nat:nature:v:432:y:2004:i:7020:d:10.1038_nature03029
    DOI: 10.1038/nature03029
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    Citations

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    Cited by:

    1. Marika K. Kucińska & Juliette Fedry & Carmela Galli & Diego Morone & Andrea Raimondi & Tatiana Soldà & Friedrich Förster & Maurizio Molinari, 2023. "TMX4-driven LINC complex disassembly and asymmetric autophagy of the nuclear envelope upon acute ER stress," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    2. Xinyu Mei & Yuan Guo & Zhangdan Xie & Yedan Zhong & Xiaofen Wu & Daichao Xu & Ying Li & Nan Liu & Zheng-Jiang Zhu, 2021. "RIPK1 regulates starvation resistance by modulating aspartate catabolism," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
    3. Aftab Nadeem & Athar Alam & Eric Toh & Si Lhyam Myint & Zia ur Rehman & Tao Liu & Marta Bally & Anna Arnqvist & Hui Wang & Jun Zhu & Karina Persson & Bernt Eric Uhlin & Sun Nyunt Wai, 2021. "Phosphatidic acid-mediated binding and mammalian cell internalization of the Vibrio cholerae cytotoxin MakA," PLOS Pathogens, Public Library of Science, vol. 17(3), pages 1-34, March.
    4. Keiji Kajiwara & Hiroshi Osaki & Steffen Greßies & Keiko Kuwata & Ju Hyun Kim & Tobias Gensch & Yoshikatsu Sato & Frank Glorius & Shigehiro Yamaguchi & Masayasu Taki, 2022. "A negative-solvatochromic fluorescent probe for visualizing intracellular distributions of fatty acid metabolites," Nature Communications, Nature, vol. 13(1), pages 1-11, December.
    5. Shiyan Liu & Mutian Chen & Yichang Wang & Yuqing Lei & Ting Huang & Yabin Zhang & Sin Man Lam & Huihui Li & Shiqian Qi & Jia Geng & Kefeng Lu, 2023. "The ER calcium channel Csg2 integrates sphingolipid metabolism with autophagy," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    6. Odeta Meçe & Diede Houbaert & Maria-Livia Sassano & Tania Durré & Hannelore Maes & Marco Schaaf & Sanket More & Maarten Ganne & Melissa García-Caballero & Mila Borri & Jelle Verhoeven & Madhur Agrawal, 2022. "Lipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    7. Smita Majumder & Arlan Richardson & Randy Strong & Salvatore Oddo, 2011. "Inducing Autophagy by Rapamycin Before, but Not After, the Formation of Plaques and Tangles Ameliorates Cognitive Deficits," PLOS ONE, Public Library of Science, vol. 6(9), pages 1-11, September.

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