. Cell heredity. Cytogenetics. 224 CELL HEREDITY. 2380 2480 2537 2650 2804 Wavelength, A 2967 FIGURE The absorption spectrum of DNA compared with the action spectrum of mutants induced by ultraviolet light. The points are for mutation in E. coli from str-d to str-s, and the curve is drawn for calf thymus DNA (from Hollaender and Zelle, 1954, First Interm. Photobiological Congress, Wageningen, Netherlands, H. Veenman and Zonen, p. 128). acids absorb the different wave lengths to different extents and, upon do- ing so, enter an excited state. The absorption spectrum of DNA is shown in Figu
. Cell heredity. Cytogenetics. 224 CELL HEREDITY. 2380 2480 2537 2650 2804 Wavelength, A 2967 FIGURE The absorption spectrum of DNA compared with the action spectrum of mutants induced by ultraviolet light. The points are for mutation in E. coli from str-d to str-s, and the curve is drawn for calf thymus DNA (from Hollaender and Zelle, 1954, First Interm. Photobiological Congress, Wageningen, Netherlands, H. Veenman and Zonen, p. 128). acids absorb the different wave lengths to different extents and, upon do- ing so, enter an excited state. The absorption spectrum of DNA is shown in Figure Superimposed on it is a curve for the number of mutations induced by the same wave lengths. This is called the action spectrum of mutation. The similarity suggests that absorption of ultra- violet light by DNA is the cause of mutation. This finding also fits the target theory well, but, again, there is reason to suspend judgment re- garding its validity. First of all, a linear relationship between ultra- violet dose and number of induced mutants is not found (Figure ). Furthermore, there is some biochemical evidence involving pre- and post- treatments of the irradiated cells which suggest that the effect of ultra- violet light is not direct. Other substances than DNA, for example RNA and the purines and pyrimidines themselves, have essentially the same absorption spectra. It could be that the initial absorption of the ultraviolet quanta occurred in these substances which exist in the cell outside of the gene. In a chemically modified form they might be in- corporated in the replicating DNA and give rise to the mutation ob- served. If this were the case, the target would be one of these sub- stances rather than the gene itself. In support of this idea is the fact that pretreatment of bacteria with purines and pyrimidines or their ribosides increases the number of mutations induced by subsequent treat- ment with ultraviolet light. On the other hand, the indirectness
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