Suppression of autophagic activity by Rubicon is a signature of aging View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Shuhei Nakamura, Masaki Oba, Mari Suzuki, Atsushi Takahashi, Tadashi Yamamuro, Mari Fujiwara, Kensuke Ikenaka, Satoshi Minami, Namine Tabata, Kenichi Yamamoto, Sayaka Kubo, Ayaka Tokumura, Kanako Akamatsu, Yumi Miyazaki, Tsuyoshi Kawabata, Maho Hamasaki, Koji Fukui, Kazunori Sango, Yoshihisa Watanabe, Yoshitsugu Takabatake, Tomoya S. Kitajima, Yukinori Okada, Hideki Mochizuki, Yoshitaka Isaka, Adam Antebi, Tamotsu Yoshimori

ABSTRACT

Autophagy, an evolutionarily conserved cytoplasmic degradation system, has been implicated as a convergent mechanism in various longevity pathways. Autophagic activity decreases with age in several organisms, but the underlying mechanism is unclear. Here, we show that the expression of Rubicon, a negative regulator of autophagy, increases in aged worm, fly and mouse tissues at transcript and/or protein levels, suggesting that an age-dependent increase in Rubicon impairs autophagy over time, and thereby curtails animal healthspan. Consistent with this idea, knockdown of Rubicon extends worm and fly lifespan and ameliorates several age-associated phenotypes. Tissue-specific experiments reveal that Rubicon knockdown in neurons has the greatest effect on lifespan. Rubicon knockout mice exhibits reductions in interstitial fibrosis in kidney and reduced α-synuclein accumulation in the brain. Rubicon is suppressed in several long-lived worms and calorie restricted mice. Taken together, our results suggest that suppression of autophagic activity by Rubicon is one of signatures of aging. More... »

PAGES

847

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-08729-6

    DOI

    http://dx.doi.org/10.1038/s41467-019-08729-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112230751

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30783089


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