고려대학교 생명과학대학 생명과학부/ 대학원 분자생명과학과

Solar irradiation including ultraviolet (UV) causes DNA and tissue damage by generating reactive free radicals which can be electrophilic or nucleophilic due to their unpaired electrons.  Little is, however, known about how free radicals induced by natural sunlight on the Earth are rapidly detected for avoidance.  We discover that Drosophila TRPA1 serves to sensitively detect photochemically active sunlight via their nucleophile sensitivity. Rapid light-dependent feeding deterrence in Drosophila was achieved by the TRPA1(A) not TRPA1(B) isoform, while they show similar electrophile sensitivities. Such isoform dependence re-emerges for structurally varying nucleophilic compounds and nucleophilicity-accompanying hydrogen peroxide (H₂O₂).  Furthermore, these isoform-dependent mechanisms converge on TRPA1(A)-specific residues, as their substitutions dramatically decreased UV, H₂O₂ and nucleophile sensitivities with electrophile responses unimpaired.  Collectively, TRPA1(A) rapidly responds to natural sunlight intensities through its cytosolic nucleophile sensitivity as a receptor of photochemically generated radicals, leading to an acute UV-induced behavioral shift in Drosophila.