Abstract
The relationship between the excision of pyrimidine dimers, host-cell reactivation and ultraviolet reactivation of phage λ has been investigated. From the kinetics of dimer excision and correlated biological effects the following conclusions are drawn. (1) Host-cell reactivation of phage λ involves the excision of pyrimidine dimers by host-cell enzymes. (2) Ultraviolet reactivation of λ does not involve enhancement of pyrimidine dimer excision. (3) In cells containing either irradiated λ DNA or irradiated bacterial DNA, host-cell enzymes preferentially excise dimers from host-cell DNA. By contrast, in irradiated cells infected with irradiated λ, dimers in λ DNA limit the excision of bacterial dimers better than the converse situation. These results suggest an unequal distribution of repair enzymes within the cell.
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