ADAPTATION TO PANTOTHENATE DEFICIENCY 22-2 



in a deficient medium, and acquire the ability to grow normally with- 

 out the added nutrilite. This appears to be due to an increase in 

 synthetic ability. For instance, Ryan (1946) has demonstrated chem- 

 ically the presence of 1 (+) leucine in the mycelium of leucineless 

 Neurospora which adapted and became able to grow in the absence 

 of leucine. 



The effect of the environment poses a problem, for the environ- 

 ment will select any spontaneously occurring variant better suited 

 to survive under the specific environmental conditions. Several 

 problems are involved in attempting to determine definitively wheth- 

 er the environment does or does not act to induce change in the or- 

 ganism. 



Critical evidence on this point was contributed by Luria and 

 Delbruck (1943) in their study of the occurrence of phage resistance 

 in Escherichia coli. A series of separate cultures of bacteria were 

 grown from an inoculum of 50 to 500 cells in the absence of phage 

 and then each entire culture was plated separately on a plate con- 

 taining phage and a study made of the number of colonies which grew 

 on each plate. 



The experiment was designed to determine (1) whether exposure 

 to phage induced the bacteria to mutate or (2) whether exposure to 

 phage merely selected mutants which had occurred spontaneously 

 prior to the exposure. If the phage induced a heritable resistance in 

 the cells, one would expect this change to be induced in approximate- 

 ly the same proportion of bacteria in a group of similar cultures, 

 except for variation due to sampling error. On the other hand, if the 

 resistant colonies were due to chance mutations, then one would ex- 

 pect a wide variation in the number of resistant cells found in each 

 culture depending on how many mutations had occurred and on the 

 time at which each mutation occurred. If a mutation occurred early 

 in the growth of the culture, by the time growth was completed there 

 would be many mutant cells in the clone derived from the early mu- 

 tation. On the other hand, if the mutation occurred near the end of 

 growth, there would be few mutant cells derived from it. This as- 

 sumes that the mutants and the original grow at the same rate. 



They found wide variation in the numbers of resistant colonies 

 and concluded from this that the resistance was caused by random 

 mutations prior to exposure to the phage. This variance test has 

 since been applied to other kinds of adaptations, including resistance 

 of Staphylococcus aureus to penicillin (Demerec 1945a, b) and sul- 

 fonamides (Oakberg and Luria 1947), mutation from histidine depen- 

 dence to independence in Escherichia coli (Ryan et al 1946) and 

 from uracil dependence to independence in Clostridium septicum 

 (Ryan et al 1946). 



However, it would be difficult to detect if phage were capable of 

 affecting or inducing mutations by this method. While the occurrence 

 of spontaneous mutations prior to exposure to the phage can account 



