Research Papers: Gerotarget (Focus on Aging):
Downregulation of protein kinase CK2 activity induces age-related biomarkers in C. elegans
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Jeong-Hwan Park1,*, Joo-Hyun Lee1,*, Jeong-Woo Park1, Dong-Yun Kim2, Jeong-Hoon Hahm3, Hong Gil Nam3,4 and Young-Seuk Bae1,2
1 School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea
2 School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea
3 Center for Plant Aging Research, Institute for Basic Science, Daegu, Republic of Korea
4 Department of New Biology, DGIST, Daegu, Republic of Korea
* These authors have contributed equally to this work
Young-Seuk Bae, email:
Keywords: C. elegans; protein kinase CK2; longevity; daf-16; Gerotarget
Received: November 02, 2016 Accepted: March 27, 2017 Published: April 07, 2017
Studies show that a decrease in protein kinase CK2 (CK2) activity is associated with cellular senescence. However, the role of CK2 in organism aging is still poorly understood. Here, we investigated whether protein kinase CK2 (CK2) modulated longevity in Caenorhabditis elegans. CK2 activity decreased with advancing age in the worms. Knockdown of kin-10 (the ortholog of CK2β) led to a short lifespan phenotype and induced age-related biomarkers, including retardation of locomotion, decreased pharyngeal pumping rate, increased lipofuscin accumulation, and reduced resistance to heat and oxidative stress. The long lifespan of age-1 and akt-1 mutants was significantly suppressed by kin-10 RNAi, suggesting that CK2 acts downstream of AGE-1 and AKT-1. Kin-10 knockdown did not further shorten the short lifespan of daf-16 mutant worms but either decreased or increased the transcriptional activity of DAF-16 depending on the promoters of the target genes, indicating that CK2 is an upstream regulator of DAF-16 in C. elegans. Kin-10 knockdown increased production of reactive oxygen species (ROS) in the worms. Finally, the ROS scavenger N-acetyl-L-cysteine significantly counteracts the lifespan shortening and lipofuscin accumulation induced by kin-10 knockdown. Therefore, the present results suggest that age-dependent CK2 downregulation reduces longevity by associating with both ROS generation and the AGE-1-AKT-1-DAF-16 pathway in C. elegans.
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