372 r. w, STAHL 



of these classes is such, that the kinetics of reactivation look one-hit, although 

 an average of 4 quanta per phage are required. Although this explanation 

 is strictly a 'posteriori, the even greater unpleasantness of possible alternative 

 explanations encourages tolerance of Bowen's suggestion. 



2. Genetic Control of Sensitivity to Ultraviolet Light 



The sensitivities of T2 and T4 differ by a factor of about two. Streisinger 

 (1956) has shown that this difference is inherited in crosses as if it were 

 controlled by a single genetic factor, the u gene. The u allele, which confers 

 resistance, may be supposed to act in one of the following ways: (1) It may 

 render the DNA of the particle intrinsically less sensitive by (a) lowering 

 the absorption coefficient for ultraviolet light, or (b) by lowering the quantum 

 efficiency for the production of lethal damages by adsorbed photons. (2) It 

 may free the phage from dependence on a set of sensitive parts of the phage 

 by rendering these parts superfluous. (3) It may be able to erase about one- 

 half of the ultraviolet-induced lesions. 



Streisinger (1956) ruled out possibility (la) by demonstrating that the 

 absorption of ultraviolet light was the same for u and w+ phage. The possi- 

 bilities (la) and (lb) are simultaneously eliminated by the following experi- 

 ment by Harm (1958b): He obtained survival curves for irradiated w+ phage 

 assayed under three different conditions: (i) on ordinary E. coli B, (ii) on 

 E. coli B infected with several particles per cell of heavily irradiated (cir. 

 140 hits) u+ phage, and (iii) on E. coli B infected with several particles per 

 cell of heavily irradiated u phage. The survival curve in the first two cases 

 was that typical of w+ phage; in the last case the curve obtained was char- 

 acteristic of u phage. 



Harm (personal communication) found that the effects of photoreactivat- 

 ing light and heavily irradiated u phage on the reduction in sensitivity of w+ 

 phage is much less than additive. The simplest explanation seems to be that 

 photoreactivating light and the u gene work by erasing classes of damages 

 which are in large part common. A similarity in action of photoreactivation 

 and the u allele is consistent with X-ray and suicide experiments. With both 

 these agents, T2 and T4 have very similar sensitivities, and very slight 

 photoreactivation, if any, can be observed. 



A detailed comparison of the radiobiology of u and u+ phage should prove 

 rewarding on two counts. It could lead to an miderstanding of the mechanism 

 of action of this interesting gene, and it could further restrict our picture 

 of T-even phage as deduced from irradiation experiments. To date, the 

 following differences have been established for u and w+ phage (either by 

 comparison of T2 and T4 or by comparison of T2w+ and T2 into which the 

 u gene has been crossed from T4): (1) The plaque-forming ability for T2 is 

 about twice as sensitive as that for T4. (2) The photoreactivable sector is 



