62 MOLECULES, VIRUSES, AND BACTERL^ 



cannot assume that the non-overlapping mutants c, h, f, g, and / are 

 point mutations; some of these, too, may involve relatively extended 

 nucleotide sequences. This is what we shall suppose. Then we shall as- 

 sume that asymmetrical results between pairs of these mutants are ob- 

 tained whenever the mutants involved are sites having distinctly dif- 

 ferent sizes. If the larger mutated site is in the recipient cell, formation 

 of wild-type recombinants is depressed. 



The question arises next as to whether the "large" mutated sites are 

 deficiencies or extended altered nucleotide sequences. Clearly, the 

 ability of a mutant to revert to wild type will not distinguish between 

 these two possibilities. If we suppose that mutants such as d and i are 

 deficiencies, and that pairing between a deficient molecule and its non- 

 deficient homologue is the same as between a deficient and non-deficient 

 chromosome, we see no reason why recombination frequencies should 

 depend on whether the deficiency is in the donor as opposed to the 

 recipient cell. If, on the other hand, we suppose that the "large" mu- 

 tated sites are not deficiencies but extended altered sequences, we can 

 construct a model which explains the asymmetries, using current no- 

 tions of negative interference. 



This model supposes the following: 



1. That pairing in the amylomaltase locus, if not in the entire DNA 

 molecule, is complete and effective. 



2. That transformation is the result of multiple cross-over events 

 in the paired region. We score as recombinant any double cross-over 

 whose effect is to substitute the normal sequence of the donor DNA 

 molecule in the chromosome for the mutated sequence of the recipient 

 cell's DNA. If the complementary event occurs, i.e., insertion of the 

 normal sequence of the recipient cell in place of the mutant sequence 

 of the donor DNA molecule, it is undetected, since the donor DNA 

 molecule, or a copy thereof, is an incomplete genome and cannot be 

 recovered in a viable cell. 



3. The first cross-over event will be supposed to occur at random. 

 It establishes the "point of attack" on the donor DNA molecule. 



4. The second cross-over event determines the point of return to 

 the recipient cell's DNA sequence, and it will be supposed to have a 

 high probability of occurring, once a point of attack has been estab- 

 lished. The points of attack and points of return define the lengths of 

 donor sequence included in the recombinant structures, and these 

 lengths fall in some kind of distribution. 



5. We shall assume that the lengths of donor sequence inserted in 

 the recombinant structures, after attacks starting at any given point, 

 are distributed normally. 



