Evidence against DNA as the target for 334 nm-induced growth delay in Escherichia coli.

Abstract

Abstract— Growth delay was induced with near‐UV (334 nm) radiation in Escherichia coli K12 bacterial strains followed by attempts at photoreactivation (PR) of this effect at 405 nm. In the UV‐sensitive strain AB2480, a small PR of the observed population growth delay occurred after 334 nm irradiation at 35°C and a much larger PR after 334 nm irradiation at 5°C. However, much of the population growth delay in this strain can be explained as being due to killing, and all or most of the observed PR pertains only to this killed fraction of the population. The true cell growth delay (i.e. that of surviving cells) thus appears to be only slightly, if at all, photoreactivable. This conclusion is supported by studies with a wild‐type strain KW8, which shows growth delay at non‐lethal doses; this growth delay shows no PR, regardless of the temperature during 334 nm irradiation. These findings indicate that photoreactivable lesions (cyclo‐butyl pyrimidine dimers) are not an important cause of near‐UV‐induced growth delay.Strain AB2480 lacks known dark‐repair systems for DNA damage induced by far‐UV (below 300 nm) radiation, yet shows the same efficiency for 334‐nm‐induced growth delay as the wild type, which possesses these dark repair systems. This indicates that lesions in DNA that are dark‐repairable by the systems not tunctional in AB2480are not responsible for 334‐nm‐induced growth delay. It is possible, however, that fragmentary repair systems in AB2480 can operate on some DNA lesion that might cause growth delay.Spontaneously decaying lesions are unlikely, since growth‐delay damage decays at a very low rate in non‐nutrient medium.Since most of the known types of DNA damage and repair are thus eliminated, these considerations suggest that DNA damage is not involved in near‐UV‐induced growth delay.