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Two derivatives of E. coli B/r having the same auxotrophic marker but differing in their ability to dark repair u.v.‐induced dimers in DNA were compared for their sensitivity to u.v.‐induced lethality and reversion to prototrophy. Ability to dark repair influenced both biological endpoints to the same extent. Thus, dimers may be primary photochemical lesions for both effects. A possible model for the system was proposed. According to this model, organisms which have more than a critical number of dimers are inactivated and organisms with the critical number or slightly fewer, survive as revertants. Post‐irradiation influences which enhance or reduce repair of dimers, in effect shift the population distribution of dimers. The result is either a net increase or decrease in the number of revertants depending upon the U.V. dose and upon whether repair is enhanced or reduced.
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Ruth F. Hill (1965) studied this question.
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