KADIOBIOLOGY OF BACTERIOPHAGE 



>63 



At each dose, the data fit these expectations. (2) Markers which are linked 

 tend to be knocked out together. The degree of correlation decreases with 

 increasing map distance between the markers. (3) The knockout of one marker 

 is correlated with a reduction in yield of a linked marker. Thus tlie ultra- 

 violet hits which knockout markers are the same as those which cause a 

 decrease in the number of copies in which a surviving marker appears. 



These observations permit the conclusion that there exists a large class 

 of ultraviolet hits which result in discrete lesions with localized effects on 

 the genetic structure of the phage. A plot of log jp versus r gives a survival 

 curve for a marker under conditions in which the survival is influenced only 

 by these "genetic" hits (Fig. 5). 

 I-Od 



10 20 



Phage-lethal UV-hits, r 



Fig. 5. The "knockout" at low doses of genetic markers in Ti by ultraviolet-induced 

 lesions on the genetic structure. Among those particles which are able to participate 

 in cross reactivation, 1 hit per 17 phage-lethal hits knocks out a given marker. The 

 values for p are from Doermann et al. (1955) and have been corrected for certain system- 

 atic errors as described by Stahl (1956). 



c. The Mechanism of Cross Reactivation. The above observations, together 

 with the obvious observation that markers from the irradiated parent tend 

 to appear in progeny particles which are genetic recombinants, tempt the 

 conclusion that the mechanism of reactivation is the separation of a marker 

 from the damages bracketing it by a process akin to, or identical to, the 

 normal process of genetic recombination. Under this interpretation the 



