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Congratulations to Dr. Shobhan Gaddameedhi, postdoctoral fellow in the laboratory of Dr. Aziz Sancar, who received the third place award at the Postdoctoral Research Poster Forum of the 2nd annual Oliver Smithies Nobel Symposium.

Shobhan Gaddameedhi, PhD (on far right)

The 2nd Annual Oliver Smithies Nobel Symposium featured a keynote talk presented by Dr. Thomas Cech (1989 Nobel laureate in Chemistry) and the 2nd annual Postdoctoral Research Poster Forum. The poster forum featured presentations from UNC fellows of all disciplines and culminated with the awarding of the best three posters presented during the symposium. All poster awardees received a signed certificate from the organizers and poster forum committee along with a monetary prize (1st place: $300; 2nd place: $200; 3rd place: $100).

Dr. Shobhan Gaddameedhi, postdoctoral fellow in the laboratory of Dr. Aziz Sancar in the Department of Biochemistry and Biophysics, received third place. His poster was entitled “Role of the Circadian Clock in UV-Induced Skin Carcinogenesis.”

Authors: Shobhan Gaddameedhi, Christopher P. Selby, and Aziz Sancar

Institution: Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill

Abstract: Skin cancer is the most common form of cancer in the United States. The main cause of this cancer is the dipyrimidine photoproducts induced in epidermal DNA by the ultraviolet (UV) component of sunlight. In mice and humans, UV photoproducts are eliminated from DNA by nucleotide excision repair (NER). Here, we describe that a rate-limiting subunit of the excision repair system, XPA, is controlled by the circadian clock in the mouse skin. As a consequence, NER exhibits daily rhythmicity in skin. The overall goal of this study is to determine whether UV exposure at certain times of the day is more likely to cause skin cancer. Skin carcinogenesis was measured in SKH-1 hairless mice that were irradiated with UV light from a sun lamp either at 4 AM or 4 PM. Measurements of protein levels, NER capacity and replication were made in control mice. Our results suggest that the XPA level and the capacity to repair UV-induced DNA damage are maximal in the evening and minimal in the morning. More importantly, we found that mice exposed to UV radiation at 4 am when repair is at its minimum are more prone to skin cancer than mice exposed to UV radiation at 4 pm when repair is at its maximum. At 25 weeks, AM treated mice had five-fold more invasive carcinomas than PM treated mice. Our studies establish a rationale for chrono-photobiological response and suggest that timing may reduce the risk of exposure to sunlight and tanning beds.