{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T21:04:30Z","timestamp":1761599070499},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,12,12]],"date-time":"2006-12-12T00:00:00Z","timestamp":1165881600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Knockout mutations in both alleles of the <jats:italic>Xpa<\/jats:italic> gene give rise to a complete deficiency in nucleotide excision repair (NER) in mammalian cells. We used transgenic mice harboring the \u03bb\u2010phage\u2010based <jats:italic>lacZ<\/jats:italic> mutational reporter gene to study the effect of <jats:italic>Xpa<\/jats:italic> null mutation (<jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) on damage induction, repair, and mutagenesis in mouse skin epidermis after UVB irradiation. UVB induced equal amounts of cyclobutane pyrimidine dimers (CPDs) and pyrimidine(6\u20104)pyrimidone photoproducts (64PPs) in mouse skin epidermis of <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and wild\u2010type mice. Neither photolesion was removed in the <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> epidermis by 12 hr after irradiation whereas removal of 64PPs was observed in the epidermis of wild\u2010type mice. Irradiation with 200 and 300 J\/m<jats:sup>2<\/jats:sup> UVB increased the <jats:italic>lacZ<\/jats:italic> mutant frequency in the epidermis of <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice, but the induced mutant frequencies were not significantly different from those previously determined for wild\u2010type mice. One\u2010hundred <jats:italic>lacZ<\/jats:italic> mutants isolated from the UVB\u2010exposed epidermis of <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice were analyzed and compared with mutant sequences previously determined for irradiated wild\u2010type mice. The distribution of the mutations along the <jats:italic>lacZ<\/jats:italic> transgene and the preferred dipyrimidine context of the UV\u2010specific mutations were similar in mutants from the <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and wild\u2010type mice. The spectra of the mutations in the two genotypes were both highly UV\u2010specific and similar in a dominance of C \u2192 T transitions at dipyrimidine sites; however, <jats:italic>Xpa<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice had a higher frequency than wild\u2010type mice of two\u2010base tandem substitutions, including CC \u2192 TT mutations, three\u2010base tandem mutations and double base substitutions that were separated by one unchanged base in a three\u2010base sequence (alternating mutations). These tandem\/alternating mutations included a remarkably large number of triplet mutations, a recently reported, novel type of UV\u2010specific mutation, characterized by multiple base substitutions or frameshifts within a three\u2010nucleotide sequence containing a dipyrimidine. We conclude that the triplet mutation is a UV\u2010specific mutation that preferably occurs in NER\u2010deficient genetic backgrounds. Environ. Mol. Mutagen., 2007. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/em.20262","type":"journal-article","created":{"date-parts":[[2006,12,13]],"date-time":"2006-12-13T00:48:46Z","timestamp":1165970926000},"page":"1-13","source":"Crossref","is-referenced-by-count":17,"title":["Mutation spectrum in UVB\u2010exposed skin epidermis of <i>Xpa<\/i>\u2010knockout mice: Frequent recovery of triplet 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