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The interplay among nucleotide excision repair, cell-cycle regulation, and apoptosis in the UV-exposed epidermis is extremely important to avoid mutations and malignant transformation. InXpc –/– mice deficient in global genome nucleotide excision repair (GGR), a cell-cycle arrest of epidermal cells in late S-phase [with near-double normal diploid (4N) DNA content] was observed 48–72 h after UV exposure. This arrest resolved without apoptosis (96–168 h). We surmised that these arrested keratinocytes with persistent DNA damage were removed by epidermal turnover.In vivo BrdUrd pulse–chase labeling (&gt;17 h after UV exposure) showed that DNA replication after UV exposure was resumed inXpc –/– mice, but it did not reveal any evidence of retained BrdUrd-labeled S-phase cells in the basal layer of the epidermis at 72 h. Interestingly, by this time a maximum number of cytokeratin 10-negative and cytokeratin 5-positive cells had appeared in the suprabasal epidermal cell layers of UV-exposedXpc –/– mice. Accumulation of these “basal cell”-like keratinocytes in the suprabasal layers was clearly aberrant and was not observed in WT and heterozygous mice. Flow cytometric analyses of single-cell suspensions from UV-exposedXpc –/– epidermis further showed that the “near-4N” arrested cells retained cytokeratin 5 and lacked cytokeratin 10. Hence, we conclude that the arrested near-4N cells became detached from the basal layer without entering a proper differentiation program and were indeed subsequently lost through the epidermal turnover. This expulsion apparently constitutes an alternative route, different fromin situ apoptosis, to eliminate DNA-damaged arrested cells from the epidermis.

Epidermal transit of replication-arrested, undifferentiated keratinocytes in UV-exposed XPC mice: An alternative to in situ apoptosis