laughnan: nature of mutations 19 



change in beta, it must be assigned to its removal altogether from the 

 complex. 



One more line of evidence, less decisive perhaps than those present- 

 ed above, may be brought to focus on the question of gene mutation of 

 the beta element, and in this case the original A h complex of Ecuador 

 origin is involved. As pointed out earlier, the elements of this com- 

 plex are ordered in reverse (a : (3) of those of the A b -P complex. More- 

 over, the alpha component of the former is isolated as a nonrecom- 

 binant with a ten-fold lower frequency compared with the corre- 

 sponding event from the A b -P complex. Among the crossover alpha 

 isolations from the A b Ja heterozygote, an occasional one is found (8) 

 that is mutable (a-m) when the Dt gene is present in the genome. 

 Kernels that carry this mutable alpha form are pale in phenotype, 

 with dots (clusters of purple cells) distributed throughout the aleur- 

 one. Since Dt is known to condition the mutation of recessive a to A 

 (18, 19) and since the mutability of the a-m derivative is also con- 

 trolled by Dt, it is inferred that a-m itself represents a complex of the 

 type a : a, in which, as a result of a crossover in the A h /a heterozygote. 

 the mutable a allele has been traded for, and taken the position of. 

 beta in the alpha: beta complex. The mutability of this new complex 

 is then considered to reside not in alpha itself but in the now adjacent 

 a element. This argument is supported by the crossover extraction of 

 the mutable a element from the a : a complex in experiments which 

 also confirm that the order of the alpha and a elements in this 

 complex, as expected, is centromere : alpha : a. 



Taking advantage of the influence of Dt on the mutation of a, 

 we have obtained from a : a homozygotes a full-colored revertant 

 whose phenotype is indistinguishable from A b . There is good reason 

 to conclude that this revertant is a synthetic A b of the type a: A, in 

 which A, originating from a as a result of mutation in situ, is substi- 

 tuted for the original beta of the complex (Figure 3). This is sup- 

 ported by tests which reveal that the revertant no longer yields a 

 derivatives and that the mutant form, in heterozygotes with recessive 

 a, yields alpha derivatives whose occurrence is associated with recom- 

 bination for the distal marker. 



The substitution of A for beta in A h affords the opportunity to 

 compare the frequencies of crossover and noncrossover alpha cases 

 from the original and the synthetic complexes. This experiment 



