VRK-1 extends life span by activation of AMPK via phosphorylation

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Vaccinia virus-related kinase (VRK) is an evolutionarily conserved nuclear protein kinase. VRK-1, the single Caenorhabditis elegans VRK ortholog, functions in cell division and germline proliferation. However, the role of VRK-1 in postmitotic cells and adult life span remains unknown. Here, we show that VRK-1 increases organismal longevity by activating the cellular energy sensor, AMP-activated protein kinase (AMPK), via direct phosphorylation. We found that overexpression of vrk-1 in the soma of adult C. elegans increased life span and, conversely, inhibition of vrk-1 decreased life span. In addition, vrk-1 was required for longevity conferred by mutations that inhibit C. elegans mitochondria! respiration, which requires AMPK. VRK-1 directly phosphorylated and up-regulated AMPK in both C. elegans and cultured human cells. Thus, our data show that the somatic nuclear kinase, VRK-1, promotes longevity through AMPK activation, and this function appears to be conserved between C. elegans and humans.
Publisher
AMER ASSOC ADVANCEMENT SCIENCE
Issue Date
2020-07
Language
English
Article Type
Article
Citation

SCIENCE ADVANCES, v.6, no.27

ISSN
2375-2548
DOI
10.1126/sciadv.aaw7824
URI
http://hdl.handle.net/10203/275807
Appears in Collection
BS-Journal Papers(저널논문)
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