| First Author | Murai H | Year | 2000 |
| Journal | Mutat Res | Volume | 450 |
| Issue | 1-2 | Pages | 181-92 |
| PubMed ID | 10838142 | Mgi Jnum | J:62686 |
| Mgi Id | MGI:1859456 | Doi | 10.1016/s0027-5107(00)00024-5 |
| Citation | Murai H, et al. (2000) Studies of in vivo mutations in rpsL transgene in UVB-irradiated epidermis of XPA-deficient mice. Mutat Res 450(1-2):181-92 |
| abstractText | We have established xeroderma pigmentosum group A (XPA) gene-knockout mice with nucleotide excision repair (NER) deficiency, which rapidly developed skin tumors when exposed to a low dose of chronic UV like XP-A patients, confirming that the NER process plays an important role in preventing UVB-induced skin cancer. To examine the in vivo mutation in the UVB-irradiated epidermis, we established XPA (-/-), (+/-) and (+/+) mice carrying the Escherichia coli rpsL transgene with which the mutation frequencies and spectra in the UVB-irradiated epidermal tissue can be examined conveniently. The XPA (-/-) mice showed a higher frequency of UVB-induced mutation in the rpsL transgene with a low dose (150 J/m(2)) of UVB-irradiation than the XPA (+/-) and (+/+) mice, while, at a high dose (900 J/m(2)) they showed almost the same frequency of mutation as the XPA (+/-) and (+/+) mice, probably because of cell death in the epidermis of the XPA (-/-) mice. However, CC-->TT tandem transition, a hallmark of UV-induced mutation, was detected at higher frequency in the XPA (-/-) mice than the XPA (+/-) and (+/+) mice at both doses of UVB. This rpsL/XPA mouse system will be useful for further analyzing the role of NER in the mutagenesis and carcinogenesis induced by various carcinogens. |
