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. 2016 Feb;38(1):27.
doi: 10.1007/s11357-016-9889-y. Epub 2016 Feb 12.

Ultraviolet-A triggers photoaging in model nematode Caenorhabditis elegans in a DAF-16 dependent pathway

Mani Iyer Prasanth  1 , Gunasekaran Santhi Santoshram  1 , James Prabhanand Bhaskar  2 , Krishnaswamy Balamurugan  3
Affiliations

Ultraviolet-A triggers photoaging in model nematode Caenorhabditis elegans in a DAF-16 dependent pathway

Mani Iyer Prasanth et al. Age (Dordr). 2016 Feb.

Abstract

Ultraviolet radiations (UV) are the primary causative agent for skin aging (photoaging) and cancer, especially UV-A. The mode of action and the molecular mechanism behind the damages caused by UV-A is not well studied, in vivo. The current study was employed to investigate the impact of UV-A exposure using the model organism, Caenorhabditis elegans. Analysis of lifespan, healthspan, and other cognitive behaviors were done which was supported by the molecular mechanism. UV-A exposure on collagen damages the synthesis and functioning which has been monitored kinetically using engineered strain, col-19:: GFP. The study results suggested that UV-A accelerated the aging process in an insulin-like signaling pathway dependent manner. Mutant (daf-2)-based analysis concrete the observations of the current study. The UV-A exposure affected the usual behavior of the worms like pharyngeal movements and brood size. Quantitative PCR profile of the candidate genes during UV-A exposure suggested that continuous exposure has damaged the neural network of the worms, but the mitochondrial signaling and dietary restriction pathway remain unaffected. Western blot analysis of HSF-1 evidenced the alteration in protein homeostasis in UV-A exposed worms. Outcome of the current study supports our view that C. elegans can be used as a model to study photoaging, and the mode of action of UV-A-mediated damages can be elucidated which will pave the way for drug developments against photoaging.

Keywords: C. elegans; IIS pathway; Lifespan; Photoaging; UV-A.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Effect of UV-A in nematode. a Confocal images showing differential regulation of col-19 in the transgenic strain TP12. b qPCR analysis showing altered expression of col-19 in wild type C. elegans. c Quantification of collagen inside the worms after exposure showing decrease in the level of collagen
Fig. 2
Fig. 2
Effect of UV-A on C. elegans lifespan. a Lifespan assay of wild type C. elegans in liquid media. Worms survived up to 15, 13, and 14 days when exposed to 2, 4, and 6 h of UV-A, respectively (p < 0.05). b Lifespan assay of wild type C. elegans in solid media. Worms survived up to 15, 15, and 10 days when exposed to 2, 4, and 6 h of UV-A, respectively (p < 0.05). c Lifespan assay of daf-2 mutant worms in liquid media. Worms survived up to 40, 35, and 30 days when exposed to 2, 4, and 6 h of UV-A, respectively (p < 0.05). d Lifespan assay of daf-2 mutant worms in solid media. Worms survived up to 42, 38, and 33 days when exposed to 2, 4, and 6 h of UV-A, respectively (p < 0.05). e qPCR expression in wild type worms showing upregulation of daf-2 and utx-1 and downregulation of daf-16 (1.18, 0.36, and 0.04 folds in 2, 4, and 6 h, respectively) during the course of exposure. Altered regulation was expressed by age-1. f qPCR expression in daf-2 mutant worms showing upregulation of daf-16 (0.98, 1.46, and 2.48 folds in 2, 4, and 6 h, respectively). However, both age-1 (5.63, 2.76, and 3.43 folds in 2, 4, and 6 h, respectively) and utx-1 (3.67, 2.37, and 2.98 folds in 2, 4, and 6 h, respectively) are showing higher fold expression than daf-16
Fig. 3
Fig. 3
Differential expression of clk-1 and eat-2 upon UV-A exposure in C. elegans. The expression of clk-1 was downregulated during the course of exposure whereas eat-2 was downregulated consistently
Fig. 4
Fig. 4
Evaluation of healthspan in C. elegans exposed to UV-A. a Pharyngeal pumping assay in C. elegans. The pharyngeal movement was reduced in worms exposed to UV-A (p < 0.05). b Brood size assay in C. elegans. The total number of eggs laid was 227, 166, and 118 in 2, 4, and 6 h exposed worms, respectively, when compared to control (314) (p < 0.05). c qPCR expression of egl-8 and egl-30 was found to be downregulated from the initial hours of exposure which showed slight upregulation during the course of exposure. In the case of dgk-1 and goa-1, it was upregulated during the initial hours which was later subsided
Fig. 5
Fig. 5
Western blot analysis of HSF-1 in wild type C. elegans. a Maximum expression was observed in 6 h exposed worms, whereas the expression was absent in 4 h exposed worms. In the case of 2 h exposed worms, the expression was meager as compared to control. b Quantification of the expressed HSF-1 was done using the ImageLab software
Fig. 6
Fig. 6
Schematic representation of initiation of photoaging by UV-A. Exposure to UV-A regulates the pivotal players of the IIS pathway, such as daf-2 (which is mediated by utx-1) along with age-1, which in turn mediates the phosphorylation and eventually blocking daf-16 from integrating into the nucleus by which lifespan was reduced. Also, the candidate players of the DAG pathway were differentially regulated, by which a reduction in healthspan was also observed. However, the other mediators of lifespan regulation, mitochondrial gene clk-1 and dietery restriction gene eat-2, were found unaffected during the course of exposure
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