220 ROBERT L. SINSHEIMER 



cistron is two or three times that of the B cistron, although the two cis- 

 trons comprise approximately equal portions of the genetic map. 



Another genetic locus which in a special circumstance has a critical 

 function is the u locus of T4. Streisinger 141 has shown that the u locus 

 of T4 is responsible for the nearly 50% reduction in ultraviolet sensi- 

 tivity of T4 phage as compared to T2 (despite their identical DNA con- 

 tent). Harm 142 demonstrated that this locus appeared to act by repairing 

 a certain fraction of the ultraviolet lesions inflicted upon T4 in a manner 

 very similar to the action of photoreactivation in T2 (T4 is only very 

 slightly subject to photoreactivation). Harm demonstrated that a single 

 heavilv irradiated T4 particle in mixed infection with ultraviolet irradi- 

 ated T2 particles could raise the level of survival of the T2 particles to 

 that of T4 particles at the same ultraviolet dose, as long as the T4 u allele 

 was effective. With very heavy doses of ultraviolet the T4 u allele itself 

 itself could be destroyed and the effect lost. 



The cross section for inactivation of the u allele — which is certainly 

 critical in this situation — as neither the T2 phage nor the T4 phage can 

 replicate until the action of the u gene repairs lesions — is about 1 % of 

 the cross section for inactivation of T4. It is thus about \i the cross sec- 

 tion of an rll A cistron. 



A recently discovered locus which, in mutant form, confers resistance 

 to proflavin inactivation, has been shown to have a cross section for ultra- 

 violet inactivation about 3% of the cross section for inactivation of T4. 

 (E. S. Edgar, personal communication). 



The apparent discrepancy between the estimates of the size of the rll 

 locus from its proportion of the genetic map and from its large relative 

 ultraviolet cross section could be reconciled in several ways. One of the 

 most appealing is to suggest that two types of ultraviolet lesions are pro- 

 duced, both of which affect function but only one of which influences 

 replication. Lesions of the first type, which are presumed to be the more 

 numerous, prevent function of a locus but permit replication to form an 

 undamaged locus. Such lesions are of no consequence if they occur in a 

 noncritical locus for which the function can be postponed until after rep- 

 lication. Lesions of either kind, however, are fatal to a critical locus. If 

 the number of critical loci is few, one will then expect such loci to be 

 several times as sensitive per unit size as the bulk of the phage genome, 

 and hence to account for an extraordinarily large fraction of the ultra- 

 violet sensitivity. 43 



The difference between the cross sections of different critical loci, how- 

 ever, cannot be explained in such a simple way and may reflect actual 

 differences in the size or ultraviolet sensitivity of the loci. 



141 G. Streisinger, Virology 2, 1 (1956). 



142 W. Harm, Natunvissenschaften 45, 391 (1958). 



