DNA replication and post-replication repair in U.V.-sensitive mouse neuroblastoma cells. 
Mouse neuroblastoma cells differentiate when grown in the absence of serum; differentiation is reversed on the addition of serum.  Differentiated cells are more sensitive to U.V.-radiation than proliferating cells.  Whereas addition of serum to differentiated neuroblastoma cells normally results in immediate, synchronous entry into S phase, irradiation just before the addition of serum results in a long delay in the onset of DNA replication.  During this lag period, incorporated 3H-thymidine appears in the light density region of CsCl gradientss, reflecting either repair synthesis or abortive replication.  Post-replication repair (gap-filling) was found to be present in proliferating cells and at certain times in differentiated cells.  It is suggested that the sensitivity of differentiated neuroblastoma cells to U.V.-radiation may be due to ineffective post-replication repair or to deficiencies in more than one repair mechanism, with reduction in repair capacity beyond a critical threshold.