Effects of Mild Heating on Recovery from Ultraviolet Inactivation in Escherichia coli B/r. I. Inhibition of Excision of Pyrimidine Dimers

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Mild heating (52℃ for 20 min) of stationary phase cells of E. coli B/r starved for 2 hr caused little killing effect (80% survival) but induced division delay (2.5 hr). When heat and UV (750 erg mm^<-2>)-treated cells were incubated in growth medium, extensive lag phase (6 hr) in cultural respose and prolonged period (4 hr) susceptible to constant level of photoreactivation were observed. Liquid holding recovery was inhibited by pre-UV heat treatment. Pyrimidine dimers in heat and UV-treated cells were not excised during 4 hr of post-incubation in growth medium. After prolonged incubation, dimer excision resumed, although the rate was much slower than in the cells treated with UV alone. It is concluded that inhibition of dimer excision plays an important role in the observed heat efects ; UV sensitization, prolongation of the period susceptible to photoreactivation, and inhibition of liquid holding recovery. Bacteria have a remarkable capacity for the repair of DNA damage induced both by far-ultraviolet light (UV) and ionizing radiation (see review 1-3). Modification of the capacity for the repair will change the sensitivity to these radiations. For example, both caffeine and acriflavine in plating agar enhance both killing and mutagenesis of E. coli presumably inhibiting excision repair (see review 4).
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