STADLER 



allele to S?" has no significance, be- 

 cause there is no way in which S" can 

 be shown to have any different rela- 

 tionship to S than to P or to any other 

 element of the complex. The same is 

 true of such a question as "Is the ele- 

 ment (D) proximal or distal to (P)?" 

 It may be proximal in one stock and 

 distal in another; in a stock in which 

 it is proximal, a short series of unequal 

 crossovers will suffice to move it to a 

 distal position. 



Although difi^erent alleles may have 

 widely different numbers of genie ele- 

 ments, none is actually a deficiency. 

 In terms of the postulated origin of the 

 cluster, all of those with more than a 

 single element may be considered dup- 

 lications. On the other hand, when we 

 arbitrarily take as the standard type 

 an allele carrying several genie ele- 

 ments, other alleles with fewer ele- 

 ments will appear as deficiencies, and 

 the mechanisms that produce them as 

 mutants from the standard type will 

 be mechanisms of gene loss. 



The same mechanisms proceeding in 

 the case of a gene-complex whose 

 separable elements are identical in ac- 

 tion might produce only a linear series 

 of multiple alleles showing various 

 grades of dilution, or they might pro- 

 duce no multiple series of alleles at all. 



The increasing number of cases in 

 which clustering of genes of identical 

 or similar effect is proved or indicated 

 (2^-27 and others, 28 and 29 for ref- 

 erences) suggests that unequal crossing 

 over may be a significant factor in the 

 production of seemingly qualitative 

 allelic differences. 



Another simplifying assumption was 

 that mutant changes in gene effect 

 must represent some transformation 

 of the gene itself rather than some al- 

 teration affecting its expression. It was 

 this assumption that made the demon- 

 stration of x-ray-induced mutation 

 and reversion of the same gene seem 



257 



critical proof of the induction of in- 

 tragenic alterations. The assumption 

 was definitely contradicted by the evi- 

 dence of position effect. This evidence 

 showed conclusively that a mutation 

 did not necessarily represent a trans- 

 formation or loss of the gene con- 

 cerned; instead, it could be the result 

 of a translocation affecting the expres- 

 sion of the unchanged gene. 



The remarkable studies of McClin- 

 tock (SO, 31) on mutational behavior 

 in maize, as affected by the introduc- 

 tion of a chromosome-9 undergoing 

 the breakage-fusion-bridge cycle, have 

 shown the far-reaching importance of 

 this limitation in the experimental 

 study of gene mutation. In the pres- 

 ence of this structurally unstable chro- 

 mosome, many of the type genes pre- 

 sent, including genes in chromosome-9 

 and genes in other chromosomes, show 

 mutation to unstable recessive forms 

 characterized by various types of chro- 

 mosomal irregularity. The study of 

 the unstable mutants and their rever- 

 sion leaves little doubt that the phe- 

 nomenon is due to some reversible in- 

 hibition of the expression of the genes 

 concerned. 



In some cases the mutations are ac- 

 companied by detectable chromosomal 

 aberrations at or near the locus show- 

 ing instability, but in other cases no 

 cytologically detectable chromosomal 

 alteration is associated with the occur- 

 rence of the mutation. In many cases 

 the instability of the recessive mutant 

 and the occurrence of the associated 

 chromosomal irregularities are de- 

 pendent upon the presence of a com- 

 plementary factor designated "acti- 

 vator" (Ac), and when this factor is 

 removed the mutant behaves as a 

 stable recessive with normal chromo- 

 somal behavior. 



McClintock has also shown that the 

 control of reverse mutation of the re- 

 cessive a by Dt (Dotted) may be a re- 



