WHAT IS A GENE? 163 



cations will remain linked on the chromosome only if there is some selec- 

 tive value to the association; otherwise we would expect them to be 

 eventually broken up through chromosomal rearrangements. Repeats 

 need not remain linked on the chromosome if the necessary organization 

 of their products can be achieved at some functioning cytoplasmic site. 

 Salmonella and E. coli, in which similar linkages have been found, may 

 not depend on cytoplasmic particles for their heterocatalytic syntheses. 

 Rather, the genes may be more directly involved, either by acting as 

 catalysts themselves or by retaining in their immediate vicinity the 

 templates or enzymes which they produce. The organized synthesis 

 may, in bacteria, take place on the genetic material itself, the organiza- 

 tion of the chromosome being maintained by selection. On the other 

 hand, it may be that in bacteria, where chromosomal rearrangements 

 have not yet been demonstrated adjacent repeats are not usually dis- 

 organized through translocation and inversion. 



How does all this relate to the explanation of pseudoallelism in terms 

 of the two hvpotheses proposed? Even genes linked in the order of the 

 sequence of reactions they control give rise to the wild, not the mutant, 

 phenotype when brought together in a diploid. Their wild-type alleles 

 need not be located on the same chromosome for their products to inter- 

 act. Furthermore, the evidence indicates that the functional gene is 

 subdivisible by mutation and recombination; this is a sufficient explana- 

 tion of the position effect observed with pseudoalleles. But how general 

 is this phenomenon? It has been observed in yeast and fungi and prob- 

 ably in higher forms. But the most extraordinary analysis of the fine 

 structure of the gene has been made in bacteriophage. 



THE STRUCTURE OF THE GENE IN BACTERIOPHAGE 



In the TA bacteriophage of E. coli there are a number of closely linked 

 genes in the r region on the map shown in Table 5.2. These so-called 

 rll genes have the function of allowing phages grown on strain B to 

 multiply normally on strain K12 after infection; mutations in these genes 

 prevent the phages from growing on strain K12. By infecting strain B 

 with equal numbers of two different rll mutants and plating the new 

 phages produced after lysis on strain K12, their relative positions in the 

 linkage group can be determined. If a recombination has occurred and 

 one of the recombinants contains the two normal alleles, it will lyse the 

 K12 bacteria and form a plaque. The ratio of plaques on K12 to the 

 count on B measures the frequency of recombinants. Infection of strain 

 B with phages of a single rll type results in the production of only very 



