48 



MOLECULES, VIRUSES, AND BACTERLV 



pect of the specificity of the gene product. We should not, therefore, 

 expect to detect as many mutational sites as there are members in the 

 sequence. Another limitation on what we shall be able to detect by 

 recombination analysis is that the detection of mutational sites will de- 

 pend not only on obtaining a mutant phenotype but also on the re- 

 combination process with which we identify the sites. If a cross is made 

 so as to confront the chromosome sequence "Mutant 1" (Figure 3) 

 with the sequence of "Mutant 2," a reciprocal exchange at one of the 

 points between the first and the fourth nucleotides indicated would 

 yield a non-mutant sequence on the one hand and a doubly mutant 

 sequence on the other. The chromosome containing the non-mutant 

 sequence would be readily detected in a selective system; the fact of 



2 



guanine 



3 



thymine 



4 

 cytosine 



5 



thymine 



adenine 

 I 

 -HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar- 



enzyme A 



determines protein A 



> detected as: 



> antigen A 



mutant 1 



guanme 



I 



guanme 



thymine 



cytosine 



thymine 



-HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar- 



determines protein A' 



> detected as: 



antigen A 



mutant 2 



adenine 



guanine 



thymine 



thymine thymine 



-HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar-HP04-Sugar- 



determines protein A' 



detected as: 

 > antigen A 



Figure 3. Schematic representation of two mutations affecting the synthesis 

 of a single gene product. Different alterations of the nucleotide sequence 

 produce different alterations of the protein structure, which render the pro- 

 tein ineffective as a catalyst. Antigenic properties being less affected by small 

 structural changes, the altered protein is often detected by its ability to react 

 with antibody directed against the normal protein. 



