Understanding the role of DAF-16 mediated pathway in Caenorhabditis elegans during UV-A mediated photoaging process

• Published in: Archives of gerontology and geriatrics 2019-05, Vol.82, p.279-285
• Main Authors: Prasanth, Mani Iyer, Venkatesh, Duraisamy, Murali, Deepa, Bhaskar, James Prabhanand, Krishnan, Venkateswaran, Balamurugan, Krishnaswamy
• Format: Article
• Language: English
• Subjects: Animals; Caenorhabditis elegans; Caenorhabditis elegans Proteins - physiology; DAF-16; daf-2 mutants; Forkhead Transcription Factors - physiology; Healthspan; Humans; Longevity; lys-7 mutants; Photoaging; Skin Aging - radiation effects; Ultraviolet Rays - adverse effects
• ISSN: 0167-4943; 1872-6976
• DOI: 10.1016/j.archger.2019.03.011

•UV-A can induce ROS inside C. elegans.•Healthspan of DAF-2 mutants were not much affected by UV-A.•DAF-16 mutants did not show any changes in lifespan when exposed to UV-A.•DAF-16 plays a key role in mediating response against UV-A. Even though Sun is the major source of energy to all living beings in the universe, continuous and prolonged exposure to sunlight will lead to detrimental effects. Human skin will undergo extrinsic aging, known as photoaging upon prolonged exposure to sunlight which is characterized by wrinkles, dryness, loss of elasticity, and so on. The model nematode Caenorhabditis elegans which is widely used in aging studies, could be used to study photoaging also. Transcription factor DAF-16, which regulates longevity, stress resistance and many other physiological events, mediates the photoaging mechanism in C. elegans. Elevation in extracellular ROS and altered expression of SGK-1 indicates the role of DAF-16 during UV-A exposure. Further, the role of daf-2, the receptor gene and lys-7, an effector gene of DAF-16 were characterized through mutant based studies. The long lived daf-2 mutants upon UV-A exposure showed reduction in lifespan, but the upregulation of daf-16 allowed the other molecular mechanisms like healthspan, antimicrobial and stress resistance to be active. In the case of lys-7 mutants, the lifespan was reduced and all other molecular mechanisms were also downregulated. However, the daf-16 mutants showed no change in lifespan irrespective of UV-A exposure. This signifies the role of DAF-16 during UV-A mediated photoaging in C. elegans. The present study helps in understanding the role of daf-16 in UV-A mediated stress response which will be of considerable importance in the field of pharmacy in designing targets for specific agents against photoaging.