The influence of growth substances upon sulphydryl compounds 



are shown in Figure 3. This work was done using acetate as a substrate. 

 Naphthalene acetic acid was appHed in varying concentrations in an effort to 

 modify the rate of acetyl ester formation. The amount of esters produced was 

 measured by the ferric hydroxamate assay. It can be seen from the figure 

 that approximately 0-5 micromoles of ester was formed in the absence of any 

 auxin, and the addition of auxin had no perceptible influence — either 

 promotive or inhibitory. The same lack of auxin eff'ect applied in the 

 absence of acetate. 



From these experiments we feel that the theory proposed by Leopold and 

 Guernsey is inadequate in its original form. 



0-^ 



I 



to 



0-7 



Acefafe acfiyafion 



-Zero time 



1-0 



I 

 0-5 % 



^ 



V 



<5i 



I 







10 



-9 



w 



10' 



/^-''M 



10''^ 10'^ 



Con en. of NAA 



Figure 3. Acethydroxamate formation with acetate activating enzyme. Final concentrations oj con- 

 stituents {after Jones et al. (1953) as in Figure 2, except CoA 

 0-2 M XHjOH. 



Incubation time: 60 minutes. 



Temperature: 30°. 



Reaction product measured according to Jones et al. (1953). 



10-" M, plus 10-2 M GSH and 



INFLUENCE OF GROWTH SUBSTANCES UPON SULPHYDRYLS 



If now we are unwilling to accept the scheme that auxins funcdon through 

 reaction with the sulphydryl of CoA, the quesdon confronts us once again as 

 to just what the role of sulphydryl compounds in growth substance action 

 might be. It is well known that iodoacetate reacts directly with sulphydryl 

 groups and in this manner inhibits a variety of enzymatic reactions essential 

 for growth. Thimann (1951) pointed out that like iodoacetate, phenyl- 

 propionic acid may inhibit enzyme sulphydryl groups and suggested an 

 analogy between this function of phenylpropionic acid and auxins. It was 

 his idea that sulphydryl inhibitors occurring naturally in the tissues might be 

 protected against by auxins. A more recent theory proposed by Muir et al. 

 (1949) included an assumpdon that auxins react with sulphydryl groups at 

 the ortko position of the ring. We would like to ask the question whether 

 auxins or growth inhibitors might in fact react with sulphydryls in vitro , in the 

 manner of iodoacetate. It might be recalled here that lactones and quinones 

 have each been considered as sulphydryl inactivating agents, and a number of 

 growth substances are of these species. 



273 



