UV-induced DNA damage in photoaging and skin homeostasis (A07)

紫外线诱导的DNA损伤促进光老化并导致皮肤癌的发展。我们已经确定，紫外线诱导的病变导致RNAPII复合体的停滞，引发了从线虫到哺乳动物的高度保守的反应程序。重要的是，反应程序增加了组织的维护，从而抵消了DNA损伤的有害后果。我们寻求理解的分子机制，协调生理调整的存在，持续的DNA损伤。

UV-induced DNA lesions promote photoaging and cause skin cancer development. We have established that UV-induced lesions that lead to stalling of the RNAPII complex elicit a response programs that is highly conserved from the nematode C. elegans to mammals. Importantly, the response program augments the maintenance of tissues and thus counteracts the detrimental consequences of DNA damage. We seek understanding of the molecular mechanisms that orchestrate physiological adjustments to the presence of persistent DNA damage.