The Proteomics of UVB radiation

Through the use of chloroflourocarbons (CFCs) contained in aerosols, the ozone layer has been depleted and presently there is a significant hole above the Antarctic. The normal function of the ozone layer is to block 97 – 99% of medium frequency ultraviolet light (200nm to 315nm), however due to the depletion, increased UV radiation through to the Earth is observed, in particular UVB (280nm – 315nm) light.

UVB is known to cause significant widespread intercellular damage through oxidative stress. However cells have shown highly organised mechanisms which attenuate and repair the damage. The authors of this study state that there are currently no studies published which quantify the proteomics of these repair system, and that the aim of this paper is to report the most significant proteins activated in this process. For this study the authors have used Photobacterium angustum, a marine gram negative deep-sea bacterium.  

Two quantitative methods were used to screen for key UVB related proteins in exponentially growing cells. A non-gel analysis was performed, consisting of post-digest isotope coded protein labelling (ICPL), which is a type of gel free mass spectrometry. In addition to this a gel based Two-Dimensional Difference Gel Electrophoresis (2D-DIGE). Using these techniques it was found that 55 proteins respond directly to UVB radiation, with RecA displaying the biggest increase in abundance (almost 3-fold). RecA is known to play a crucial role in the recombination repair process of damaged DNA, and therefore it’s upregulation after UVB damage to DNA is logical.

Overall the proteins stimulated by UVB radiation provide an intercellular pathway network (Figure 1) in which the authors suggest nutrient exchange and stabilisation of the structure of the cell is facilitated. However the transcription and translation of these proteins is very tightly regulated to avoid too much repair and therefore morphological change. Less obviously, oxidative stress repair mechanisms are also activated, at relatively high cost to the cell. Thus indicating a link between UVB radiation and oxidative stress in other parts of the cell than the nuclear DNA. However the author offers no suggestions as to where or what is damaged in addition. In summary this highly responsive system allows for rapid replacement of damaged cellular components.

The significance of this study is disputable. Whilst it is easy to admit that, with the high commercial use of sunbeds and the depletion of the ozone, UV radiation (and therefore skin cancer) is becoming an increasingly mainstream problem and therefore a primary proteomics study into the cellular effects of UV radiation is required. However these exact results are almost common sense as it is well known that UV radiation causes oxidative damage to DNA and therefore it is expected that DNA repair enzymes are activated. Nevertheless this study has allowed the exploration of the technical aspect of quantitative proteomics methodology, and from this first building block, new insights into DNA damage related diseases, such as cancer, may be found.

REFERENCE: Matallana-Surget S., Joux F., Wattiez R., Lebaron P. (2012) Proteome Analysis of the UVB-Resistant Marine Bacterium Photobacterium angustum S14, PLoS One. 7, (8). 

Accessed from:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411663/