In Escherichia coli K12 the reactivation of UV-irradiated phage in UV-irradiated cells (Weigle reactivation) is inhibited if the protein synthesis inhibitor chloramphenicol is present during the post-irradiation incubation. In contrast, in E. coli K12 or Salmonella typhimurium LT2 containing the plasmid pKM101 the kinetics of the W-reactivation response were not affected by chloramphenicol. Under the conditions used, protein synthesis was greater than 99% inhibited and no preferential synthesis of plasmid-coded proteins was apparent in the residual protein synthesis. This increased capacity to reactivate irradiated phage decayed over 2 h if the cells were allowed to grow but was relatively stable if they were incubated in 10 mM MgSO4. Whereas the capacity of UV-irradiated bacteria with or without pKM101 to carry out W-reactivation had largely decayed by the end of a 2 h post-irradiation incubation in minimal-glucose with chloramphenicol, the capacity to synthesize high levels of the recA protein had not. Post-irradiation treatment with chloramphenicol did not abolish the UV-protective effect of pKM101 or R46. pKM101-mediated W-reactivation is recA+-dependent in S. typhimurium and recA+ lexA+-dependent in E. coli K-12. The inefficiency of S. typhimurium LT2 relative to E. coli in carrying out W-reactivation is not due to the presence of the cryptic plasmid in the LT2 strains. Two possible models are discussed.