Understanding the role of p38 and JNK mediated MAPK pathway in response to UV-A induced photoaging in Caenorhabditis elegans

Premature aging of the skin, principally induced by the UV radiations is called as photoaging, characterized by an increase in the level of ROS and the damage of the collagen layer leading to the damage of the cells. Mitogen activated Protein kinase (MAPK) pathway is known to mediate photoaging by controlling the level of ROS and initiating detoxification. Caenorhabditis elegans, a known model to analyze photoaging was used to understand the role of MAPK pathway (p38 and JNK) during UV-A mediated photoaging. Gene specific mutants of p38 MAPK pathway showed reduced survival when exposed to UV-A suggesting that UV-A mediated photoaging was dependent on this pathway. Also, the role of SKN-1 in eliciting response against UV-A was analyzed with the help of GFP tagged strains and qPCR analysis. Further, UV-A did not have any impact on the lifespan of JNK pathway mutants suggesting the importance of the pathway in eliciting a response against UV-A exposure, which was further validated by Western blot analysis. Overall, this study suggests that MAPK pathway could play an important part in initiating and eliciting a response by the host against UV-A exposure, by which it could be used as a marker to analyze the effects of photoaging. •Phosphorylation of MAPK induces photoaging.•JNK MAPK is essential to initiate response during photoaging in C. elegans.•SKN-1 elicits response against UV-A mediated photoaging.•MAPK can act along with DAF-16 in mediating photoaging.