276 Auxins in Agriculture 



tabolism induced by the presence of large amounts of auxin. They 

 suggested that such toxic substances might be either lactone com- 

 pounds or perhaps amino acids or other protein fragments. It is well 

 known that subsequent to 2,4-D application, large quantities of amino 

 acids do accumulate in some plant parts (Sell et al, 1949). Accumula- 

 tions of a toxic lactone compound, scopoletin, have also been observed 

 to occur following 2,4-D application in some susceptible plants (Fults 

 and Johnson, 1950). 



Another suggestion by Bonner and Bandurski (1952) was that 

 herbicidal action may be a result of the activation of phosphatase 

 systems. Such an activation might lead to the destructive hydrolysis 

 of high-energy phosphate bonds, resulting in a considerable increase 

 in catabolic activity which could essentially prevent growth or anabo- 

 lism in the cell. Some evidence that auxins and some related com- 

 pounds may alter high-energy phosphate systems was discussed in 

 chapter VIII. Supporting evidence for such a mode of action comes 

 from the work of Loustalot et al (1953) indicating that large amounts 

 of inorganic phosphate appeared in bean plants as the lethal action 

 of 2,4-D set in. Such increases are just what one might expect if 

 phosphatase activity were involved in the herbicidal function. 



It has been suggested by Northen (1942) that the essential action 

 of auxins may be an hydrolysis of protein materials in the cell. Auxins 

 generally bring about a decrease in the viscosity of cell cytoplasm 

 which may be a reflection of protein hydrolysis. High concentrations 

 of auxin may cause extreme hydrolysis and retard or destroy essential 

 enzymatic activities. It may be that the increases in amino acids ob- 

 served by Sell et al (1949) are a consequence of such an hydrolytic 

 action. 



Another suggestion about the possible mechanism of herbicidal 

 action of auxins is the suggestion by Rhodes et al (1950) that auxins 

 may kill by interference with potassium metabolism. The initial ob- 

 servations which led to this suggestion are cited in figure 62 (p. 135). 



It seems entirely possible that the herbicidal action of auxin is a 

 combination of several of these functions or other functions yet to be 

 discovered, and in different situations any one of them may be 

 responsible for the herbicidal effect. Thus some plants may finally 

 succumb as a result of destruction of the phloem, others from the 

 accumulation of toxic materials or depletion of mobile phosphate 

 energy or to combinations of any of these. The reader will recognize, 

 however, that no satisfactory explanation of auxin toxicity has yet 

 been proposed and supported by convincing experimental evidence. 



