부산대학교 도서관

Two mechanisms proposed to explain post-replication repair of DNA strand breaks in mammalian cells are discussed. The gapped synthesis model predicts that daughter strands replicated on damaged templates will contain discontinuities. The size of the nascent strands should be equal to the distance between the damages. Moreover, the rate of fork movement should be independent of the rate of discontinuity repair. The replicative bypass model predicts that there will be no discontinuities in the daughter strands. Blocking repair would prevent fork movement. The experiments reported using cultured Chinese hamster cells were performed in order to distinguish between these two mechanisms.