ULTRAVIOLET ACTION SPECTRA FOR DNA DIMER INDUCTION, LETHALITY, AND MUTAGENESIS IN Escherichia coli WITH EMPHASIS ON THE UVB REGION

Abstract

Ultraviolet (UV) action spectra were obtained for lethality and mutagenesis (reversion to tryptophan independence) in Escherichia coli WP2s for wavelengths 254405 nm with detailed analysis in the UVB region (290-320 nm). Parallel chemical assay yields of pyrimidine dimers in DNA of E. coli RT4 were determined at the same wavelengths. Spectral regions isolated from a Xe arc and resonance lines from a high-pressure Hg-Xe arc lamp were both used for irradiation. In all cases, precise energy distributions throughout the isolated Xe bands regions were defined.Lethality, mutagenesis, and dimer induction all decreased in efficiency in a similar fashion as the wavelengths of the radiation increased. Between 300 and 320 nm, all characteristics measured showed differences of about two and a half orders of magnitude. Between these wavelengths, the values of the thrcc end points used either coincide with or parallel the absorption spectrum of DNA. The mutagenesis action spectrum coincides closely with the absorption spectrum of DNA. The lethality spectrum is closely parallel to the mutagenicity spectrum; the points, however, consistently occur at about 2 nm longer wavelengths. A calculation derived from the slope of the UVB spectra reveals that a I-nm shift of the solar UV spcctrum, to shorter wavelengths would result in a 35% increase in its mutagenic potential. At 325 nm, both biological action spectra show sharp decreases in slope. In addition, above 325 nm the spectra for lethality. mutagenicity, and dimer formation diverge sharply; lethalities at these UVA wavelengths were approximately tenfold greater relative to mutagenicity than at shorter wavelengths. The relative yield of dimcr formation by 365 nm radiation is intermediate between the yields for lethality and mutagenesis.

Ground-Based Observation of Biologically Active Solar Ultraviolet-B Irradiance at 35.DEG.N Latitude in Japan.

“…The measurement of killing efficiency on bacteriophage T 1 has been described previously . The inactivation UV action spectrum of the bacteriophage T 1 is very similar to the biological action spectra such as the dimer formation in DNA (PEAK et al, 1984), the lethality and mutagenesis of E. coli (PEAK et al, 1984), the inactivation of various cells (JAGGER, 1985), and the DNA absorption (SETLOW, 1974;SUTHERLAND and GRIFFIN, 1981). In the upper panel of Fig.…”

Photoreactivation in phr mutants of Escherichia coli K-12

“…A third possibility is that pyrimidine dimers are directly reversed by black light. Extensive literature exists indicating that black'light actually introduces pyrimidine dimers in DNA (10,26,27), and therefore it is difficult to imagine how a probably very inefficient photoreversal process would increase cell survival by use of light that introduces more dimers into DNA. In conclusion, we have no satisfactory explanation at present for the residual photoreactivation activity observed in phr mutants.…”

Site and strand specificity of UVB mutagenesis in the SUP4-o gene of yeast.

“…Although UVB wavelengths also produce these two types of photoproduct (6,(10)(11)(12), other lesions such as DNA strand breaks and thymine glycols are induced by UVB treatment (13,14). The precise roles of these various lesions in UVB mutagenesis, and thus the mechanism(s) involved, have yet to be established.…”

“…The precise roles of these various lesions in UVB mutagenesis, and thus the mechanism(s) involved, have yet to be established. There is evidence implicating cyclobutane dimers and (6-4) photoproducts in the mutagenicity of UVB radiation (12,15), but there also are indications that the nondimer lesions may contribute significantly (6,15). To add to the complexity of this situation, other factors may influence the production of UVB-induced mutations.…”