Characteristics of DNA Excision Repair in Nondividing Xeroderma Pigmentosum Cells, Complementation Group C

Abstract

Most of the cells in the human body are relatively quiescent, entering an active cell division cycle infrequently or in some cases not at all during the life span of an individual. In contrast, most studies of radiation effects and DNA repair mechanisms in human cells are done with cultured cell populations maintained in an active, proliferative state. In response to this contradiction, we have studied cultures of quiescent cells that exhibit the low levels of DNA replicative synthesis and cell division found in human skin. We find that radiation, in particular ultraviolet light (UV;240 to 313 nm) and sunlight, produces changes in the quiescent cells that can be readily observed and quantified. DNA is the principal target for these changes and DNA excision repair can ameliorate them (Kantor, 1986). Studies employing cells that are deficient in DNA excision repair from patients with the genetic disease xeroderma pigmentosum (XP) have been useful in defining the molecular basis for these changes. Here we describe results obtained with XP cells from complementation group C (XP-C) that further extend our understanding of the cellular reaction to UV and of DNA excision repair processes and their significance in human cells.