Opsin 3 mediates UVA-induced keratinocyte supranuclear melanin cap formation

Solar ultraviolet (UV) radiation-induced DNA damage is a major risk factor for skin cancer development. UV-induced redistribution of melanin near keratinocyte nuclei leads to the formation of a supranuclear cap, which acts as a natural sunscreen and protects DNA by absorbing and scattering UV radiation. However, the mechanism underlying the intracellular movement of melanin in nuclear capping is poorly understood. In this study, we found that OPN3 is an important photoreceptor in human epidermal keratinocytes and is critical for UVA-mediated supranuclear cap formation. OPN3 mediates supranuclear cap formation via the calcium-dependent G protein-coupled receptor signaling pathway and ultimately upregulates Dync1i1 and DCTN1 expression in human epidermal keratinocytes via activating calcium/CaMKII, CREB, and Akt signal transduction. Together, these results clarify the role of OPN3 in regulating melanin cap formation in human epidermal keratinocytes, greatly expanding our understanding of the phototransduction mechanisms involved in physiological function in skin keratinocytes. The G protein-coupled receptor Opsin 3 is critical for supranuclear cap formation mediated by solar ultraviolet radiation in human epidermal keratinocytes.

Automated summary

This study reveals that OPN3 is an important photoreceptor in human epidermal keratinocytes, and it is critical for the formation of supranuclear cap mediated by UVA. OPN3 mediates the formation of supranuclear cap through the calcium-dependent G protein-coupled receptor signaling pathway, which ultimately upregulates the expression of Dync1i1 and DCTN1 in human epidermal keratinocytes by activating calcium/CaMKII, CREB, and Akt signal transduction. These findings greatly expand our understanding of the phototransduction mechanisms involved in physiological function in skin keratinocytes.