Open Close
Nakamura, S., Oba, M., Suzuki, M., Takahashi, A., Yamamuro, T., Fujiwara, M., Ikenaka, K., Minami, S., Tabata, N., Yamamoto, K., Kubo, S., Tokumura, A., Akamatsu, K., Miyazaki, Y., Kawabata, T., Hamasaki, M., Fukui, K., Sango, K., Watanabe, Y., Takabatake, Y., Kitajima, T.S., Okada, Y., Mochizuki, H., Isaka, Y., Antebi, A., Yoshimori, T. (2019). Suppression of autophagic activity by Rubicon is a signature of aging.  Nat. Commun. 10(1): 847.
FlyBase ID
Publication Type
Research paper

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.

PubMed ID
PubMed Central ID
PMC6381146 (PMC) (EuropePMC)
Associated Information
Associated Files
Other Information
Secondary IDs
    Language of Publication
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Nat. Commun.
    Nature communications
    Data From Reference