The accurate process for repairing crosslinks is homologous recombinational repair (HRR). This involves replacing the damaged information using the intact information from another homologous chromosome in the same cell. "Escherichia coli" cells deficient in HRR are highly sensitive to PUVA compared to wild-type cells. HRR appears to be efficient. In "E. coli", even though one or two unrepaired crosslinks are sufficient to inactivate a cell, a wild-type cell can repair and therefore recover from 53 to 71 psoralen crosslinks. In the yeast "Saccharomyces cerevisiae" HRR is a major pathway for accurately removing psoralen-crosslinks. In wild-type yeast, the recombination events associated with crosslink removal by HRR are predominantly non-crossover gene conversion events. Psoralen crosslinks in virus DNA also appear to be removed by a recombinational repair process as occurs in SV40 virus infected cells, and in herpes simplex virus infected cells.