33. NUCLEIC ACIDS OF THE BACTERIAL VIRUSES 219 



discrete regions of the DNA structure and that at least certain types of 

 ultraviolet damage can prevent not only the function of a DNA segment 

 but also its replication per se or in a recombination event. 



The significance of the cross section for inactivation of a locus (relative to the 

 cross section for inactivation of an entire particle) is dependent in part upon the 

 physical size of an individual ultraviolet-induced lesion and the influence of such 

 lesions upon genetic recombination at nearby locations along the genetic map. Bari- 

 celli 41 has computed, from the multiplicity reactivation data of Luria and Dul- 

 becco, 48 ' 49 that an ultraviolet lesion of a noncritical locus effectively destroys a 

 length of chromosome equivalent to 0.3 to 0.4% of the total chromosome map. By 

 destruction is meant that this entire segment of chromosome is effectively a damaged 

 area for the process of multiplicity reactivation which presumably involves a recom- 

 bination of undamaged units of two or more phages to provide an intact genome. For 

 multiplicity reactivation to be possible an equivalent length of undamaged genetic 

 material at an equivalent site on another chromosome must be available. 



From the initial rate at which genetic markers are made unavailable by ultraviolet 

 irradiation to cross-reactivation, one could naively compute a cross section for this 

 process of about 4% of the cross section of phage inactivation. 50 However, any at- 

 tempt to use these data to estimate the fraction of the genome occupied by a specific 

 locus involves complex assumptions about the nature of the cross-reactivation 

 process, the fraction of the locus that is essential for cross-reactivation, and so forth, 

 and such attempts have not produced generally accepted results. 



It would seem possible, however, to arrive at a better estimate of the 

 size of a functional locus by experiments designed to measure the rate 

 of inactivation of critical loci, loci that must function before replication 

 and recombination. 



The A and B cistrons of the rll locus appear to be critical in this sense 

 for infection by r mutants in E. coli K12 (X) (they are not critical in this 

 sense for infection by r mutants in E. coli B). 42 ' 43, 136 Krieg 43 has deter- 

 mined that the cross section of ultraviolet inactivation of the function 

 of the A locus (measured by the failure of a mixed infection in K12 (X) 

 of an irradiated rll + phage and an rll A mutant) is 0.10, of the cross section 

 for free phage inactivation, while the corresponding cross section for the 

 B locus is 0.05. The two loci are inactivated together more frequently 

 than would be anticipated by chance. If Baricelli's estimate of the size 

 of ultraviolet damage is even approximately correct, this latter result could 

 not be the result of a single lesion overlapping into both cistrons, but 

 seems more likely to be the result of a fraction of less specific ultraviolet 

 damages that may, for instance, completely prevent the entire genome 

 from participation in infection. If an attempt is made to subtract this 

 putative class of lesions, the total cross section remaining for the A and 

 B cistron is still about 0.08 of that of the entire phage. This may be com- 

 pared with the estimate that the A and B loci comprise about 0.02 of 

 the genetic map. The corrected cross section for inactivation of the A 



