REGULATION 



143 



genetic experiments established that the mutation to respiration deficiency 

 does not concern a chromosomal gene. It must consist in the loss or 

 irreversible inactivation of an extrachromosomal factor which is necessary 

 for the synthesis of respiratory enzymes (Chen et ah, 1950). This extra- 

 chromosomal factor is perpetuated during cell proliferation, since it is 

 transmitted indefinitely through generations in normal yeast. 



Crosses involving the 'suppressive' type of small colony mutant give a 

 slightly different picture. Zygotes formed by fusion of a normal with a 

 suppressive are able to respire and they can be made to sporulate. 



But in this case, the four spores in each ascus all produce respiratory 



Fig. 35. Result of a cross between a normal strain (G) and a cytoplasmic 



mutant (P) of yeast. The capacity to form respiratory enzymes is indicated 



by stippling (Ephrussi, 1953). 



deficient mutants which are of the suppressive type. Here again the 

 respiration capacity fails to segregate as mendelian markers do, indicating 

 that it depends for its transmission on an extrachromosomal factor. This 

 time, the small colony character prevails; it would seem that the sup- 

 pressive mutant not only fails to perpetuate the normal extrachromosomal 

 object, but that it also prevents its reproduction in the cytoplasm of the 

 hybrid. 



Comparable observations were made on Neurospora crassa, for the 

 synthesis of the same group of respiratory enzymes. Several respiration 

 deficient mutants were isolated by Mitchell and Mitchell (1952). Some of 



