WEED control: applied botany 417 



fall into a wide array, ranging from purely physical mechanisms, wherein the 

 regulator, by affecting surface relations, changes interfacial activity at the 

 plasma membrane to chemical mechanisms involving salt or amide linkages 

 with a protein. Leopold (1955) lists five possible mechanisms of toxic action 

 of auxin-like herbicides: (1) respiratory depletion, (2) cellular proliferation, 

 (3) formation of toxic materials, (4) an activation of phosphate metabolism, 

 and (5) hydrolysis of proteins. In view of the specificities that have been 

 demonstrated and the known relations of structure to function for growth 

 regulators, it seems probable that definite molecular configurations are in- 

 volved in herbicidal action and that chemical and physical binding of the 

 toxicant with a substrate are involved. Between this reaction at the molecular 

 level and the final herbicidal response by whole plants, many secondary 

 effects may be interposed: cell proliferation, phloem plugging, mitotic aber- 

 rations, metabolic disturbances of many types, and even invasion of tissues 

 by fungi and bacteria. In seeking answers to the many questions that arise 

 in the interpretation of iield results with herbicides, one cannot afford to 

 overlook any of these effects. Undoubtedly singly or in combination they are 

 responsible for weed killing. One thing seems certain. For compounds having 

 the profound effects on plants that the hormone-like herbicides do, the 

 primary action must take place early in the over-all process of metabolism. 

 Such a process is the one involving oxidation of acetaldehyde to acetic acid 

 and concurrent reduction of acetaldehyde to ethanol mentioned by Freed 

 and Remmert (1956). These reactions are shown to be sensitive to 2,4-D in 

 vitro. 



Since 1944 the bulk of the research on mode of action of herbicides has re- 

 volved around the chlorophenoxy acetates. Other work has been done, how- 

 ever, that is worthy of mention. 



Ivens and Blackman (1949) report that the carbamates disrupt mitosis in 

 roots of barley and peas. Concentrations that inhibited root extension upset 

 cell division and produced nuclear abnormalities. Trichloroacetic acid and 

 its salts have profound formative effects on plants, and they seem to affect 

 top growth more than root tissue. The same can be said of the newer mate- 

 rial Dalapon (sodium dichloropropionate). AT'- 1-naphthylph thalamic acid, in 

 addition to being extremely toxic to many plants, destroys the mechanism 

 of geotropism of roots so that they grow upward and may protrude above 

 the soil level. 



The substituted ureas, such as 3- (/>-chlorophenyl)- 1,1 -dimethyl urea, are 

 absorbed principally from the soil by roots. After considerable top growth 

 has been made, the shoots start dying back from the tips. Leaves of trees show 

 a mottled chlorosis. Freed (1952) has suggested that nitrogen metabolism is 

 disturbed. 



Maleic hydrazide applied as a spray throws plants into a dormancy which. 



