Abstract— Near‐ultraviolet radiation (near UV; 300–380 nm) has long been known to produce a transient reduction of the capacity of bacteria to support phage growth. The present work shows that, at high fluenœs (40–100 kJ/m2), 85% of 334‐nm‐induced reduction of capacity in Escherichia coli B/r requires the rel gene; that is, it results from rel‐gene activity caused by the near‐UV treatment. This rel‐gene activity leads to (1) a bacterial growth delay and concomitantly lowered bacterial metabolism, and (2) a parallel delay in phage development, with a considerable depression of burst size. We propose that the observed effects on phage development are a consequence primarily of the lowered bacterial metabolism, but they may also result partly from a direct inhibition of phage DNA synthesis by the rel gene product, these effects together leading to the observed reduction of capacity in a rel+ strain. The remaining 15% of capacity reduction, observed in a rel strain, has an unknown mechanism, but does appear to involve a delay in phage development. At least 95% of the total capacity reduction observed in the rel+ strain in the range 40–100 kJ/m2 requires the presence of 4‐thiouridine, an unusual base in E. coli transfer RNA, which is presumably both the chromophore and the target for near‐UV‐induced capacity reduction.

Near-ultraviolet radiation (near UV; 300-380 nm) is known to inhibit the induced synthesis of tryptophanase by tryptophan in Escherichia coli, showing an action spectrum similar to that for near-UV-induced growth delay. The present work shows that a relA mutant of E. coli B/r exhibits 50% as much monochromatic near-UV (334 nm) inhibition of tryptophanase induction as the wild type, and tht a mutant lacking 4-thiouridine, an unusual nucleoside in tRNA, exhibits greater than 10% as much inhibition of tryptophanase induction. These findings indicate that 4-thiouridine is almost the sole chromophore for this effect in E. coli B/r, but that only 50% of the effect operates by a mechanism utilizing the relA(+) gene product; growth delay appears not to be primarily involved.

No abstract