Du Eun Jo, Ahn Tae Jung, Wen Xianlan, Seo Dae-Won, Na Duk L, Kwon Jae Young, Choi Myunghwan, Kim Hyung-Wook, Cho Hana, Kang KyeongJin
Samsung Biomedical Research Institute, Seoul, Republic of Korea.
Department of Anatomy and Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Elife. 2016 Sep 22;5:e18425. doi: 10.7554/eLife.18425.
Solar irradiation including ultraviolet (UV) light causes tissue damage by generating reactive free radicals that can be electrophilic or nucleophilic due to unpaired electrons. Little is known about how free radicals induced by natural sunlight are rapidly detected and avoided by animals. We discover that Transient Receptor Potential Ankyrin 1 (TRPA1), previously known only as an electrophile receptor, sensitively detects photochemically active sunlight through nucleophile sensitivity. Rapid light-dependent feeding deterrence in was mediated only by the TRPA1(A) isoform, despite the TRPA1(A) and TRPA1(B) isoforms having similar electrophile sensitivities. Such isoform dependence re-emerges in the detection of structurally varied nucleophilic compounds and nucleophilicity-accompanying hydrogen peroxide (HO). Furthermore, these isoform-dependent mechanisms require a common set of TRPA1(A)-specific residues dispensable for electrophile detection. Collectively, TRPA1(A) rapidly responds to natural sunlight intensities through its nucleophile sensitivity as a receptor of photochemically generated radicals, leading to an acute light-induced behavioral shift in .
包括紫外线(UV)在内的太阳辐射通过产生具有未成对电子的亲电或亲核活性自由基来导致组织损伤。关于动物如何快速检测并避免自然阳光诱导的自由基,我们知之甚少。我们发现,瞬时受体电位锚蛋白1(TRPA1),此前仅作为一种亲电受体为人所知,它通过亲核敏感性灵敏地检测光化学活性阳光。在[具体动物]中,快速的光依赖性摄食威慑仅由TRPA1(A)亚型介导,尽管TRPA1(A)和TRPA1(B)亚型具有相似的亲电敏感性。这种亚型依赖性在检测结构多样的亲核化合物和伴随亲核性的过氧化氢(HO)时再次出现。此外,这些亚型依赖性机制需要一组对于亲电检测可有可无的共同的TRPA1(A)特异性残基。总体而言,TRPA1(A)通过其作为光化学产生的自由基受体的亲核敏感性,对自然阳光强度做出快速反应,导致[具体动物]出现急性光诱导行为转变。