BACTERIOPHAGE GENETICS 311 



found that the double recombinants were twenty to thirty times as frequent 

 as would be predicted if the recombinational events were independent. 

 This same result has been obtained with very closely linked markers in other 

 organisms, and a variety of explanations have been proposed. One proposal 

 is that switching events to produce recombinants occur in clusters along the 

 hnkage map. These clusters are not ordinarily observed as such, since if the 

 markers used are distant compared to their size, only those which contain 

 an odd number of switches produce recombinants. The analysis of the data 

 in terms of these clusters is not yet complete (Barricelli, 1958), but prelim- 

 inary results indicate that the mean number of switches per cluster may have 

 to be only slightly higher than one to account for the observed results, 



VIII, Phenotypic Variations 



A. Phenotypic Mixing 



In general, when a single phage particle infects a cell, the new phage 

 particles produced are, except for the very rare mutant, identical with the 

 infecting particle. It is, in fact, this stability of the phage's characteristics 

 which makes possible the study of its genetics. There are, however, three 

 known exceptions to this general rule. Cells singly uifected with heterozygous 

 particles are effectively mixedly infected, since they yield two progeny types 

 as well as a few more heterozygotes which may be newly formed. 



The output of a phage cross can contain, in addition to the heterozygotes, 

 a second type of confused particle called phenotypically mixed (Novick 

 and Szilard, 1951). These are genetically pure, since the plaques they produce 

 contain phage which is all of the same type. However, they do not show the 

 same phenotypic character when they first arise in the cross that they show 

 after they have grown through one cycle in a new bacterium. Phenotypic 

 mixing does not occur for all genetic markers; it seems to be Hmited to those 

 which affect the protein coat of the phage, for example, the h mutants, 

 which control the ability of the coat protein to attach to the bacterial surface. 

 The explanation of this phenomenon, which fits all the currently available 

 data, is that the molecules which wiU form the protein coats are made by all 

 the genetic structures which are in the infected ceU, and there is a random 

 assortment of these new molecules with the genetic material at the time of 

 maturation. Thus, one can explain the finding (Streisinger, 1956) that the 

 phenotypic character of a particle liberated in a cross is determined more by 

 the majority type in the cross than by the genetic characteristic of the particle. 

 If this explanation is correct, then the phenomenon of phenotypic mixing is 

 relevant to the problem of how the genetic material acts in making protein, 

 but is not relevant to the problem of how recombinants are made. 



