Title: PHOTOREACTIVATION SPECTRA FOR PROPHAGE-INDUCING UV DAMAGE AND DELAYED APPEARANCE OF INDUCED PROPHAGE IN <i>ESCHERICHIA COLI</i>
Abstract: Various treatmentsare known to modify the frequency of prophage induction by ultraviolet radiation (UV) in Escherichia coli.Recently (Harm 1965 ; Van de Putte et al. 1967 ;Howard-Flanders 1966) it has been found that UV lesions responsible for inducing prophage in E. coli are susceptible to dark repair in cells.Prior to this finding, evidence has already accumulated that UV-induced lethal lesions are primarily pyrimidine dimers and that these dimers are repaired by an excision-resynthesis repair system or reversed to monomers photochemically by the catalysis of photoreactivating enzyme available in normal strains of E. coli (see, e.g., review of J. K. Setlow 1966).From action spectrum studies of photoreactivation (PR) of mutational damage, it was concluded (Kondo and Jagger 1966;Kondo and Kato 1966) that pyrimidine dimers are the major cause of UV-induced mutation to prototrophy in E. coli.As suggested by these findings, pyrimidine dimers may also be the major cause of prophage induction.If so, action spectra for PR should be of the same shape for these three biological responses.The initial part of the present paper describes the action spectra for PR of prophageinducing lesions in two E. coli strains possessing and lacking PR enzyme activity.