Abstract
UV induces DNA lesions such as cyclobutane pyrimidine dimer (CPD), which can cause genetic mutations. Organisms have preventive measures for DNA lesions such as translesion DNA synthesis (TLS), which keeps DNA synthesis from being blocked by the lesions. Xeroderma pigmentosum (XP) variant group (XPV) is deficient in the Polh gene, which encodes one of the TLS-specific DNA polymerases, pol η. In this study, we attempted to clarify the roles of pol η in protecting the skin from harmful influences caused by UVB (280~320 nm), using XPV model mice. We prepared the XPV model mice (Polh-/-) harboring E. coli LacZ transgenes by mating lacZ-transgenic mice and Polh-knockout mice. After UVB irradiation (0~1 kJ/m2) to the mice, the exposed skin was removed, genomic DNA was extracted and the lacZ transgenes were recovered. Then we examined the mutant frequency of the transgene with a bacterial genetic assay. We also analyzed the mutation spectrum by DNA sequencing of the mutant lacZ genes recovered in the assay. The significance of the obtained results will be discussed.
