Chemical structure and biological activity 



growth), while leaving its antagonistic effects against externally applied 

 auxin intact. However, other explanations may also be possible. 



Once the possibility of a competitive inhibition of the auxin effects is 

 accepted, the next step is to inquire into the existence of substances inter- 

 mediate between the typical auxins and the typical anti-auxins (cf Aberg, 

 1952). The molecules of such a substance should have a conspicuously 

 decreased, though not totally eliminated activity in initiating the auxin 

 responses when JDOund at the proper sites. For the sake of brevity we will 

 denote an activity defined in this way as 'intrinsic auxin activity'. We then 

 have to differentiate between three different ways of defining the activity of a 

 certain regulator as related to a specified growth result : 



(i) The 'gross activity' (i.e. secondary activity of Went and Thimann, 1937), 

 expressing the relation between growth result and external amount or 

 concentration of applied regulator; it is conditioned by the 'primary 

 activity' of the regulator and also by such factors as penetration, transport, 

 and destruction. 



(ii) The 'primary activity' (Went and Thimann, 1937), defined in 

 relation to the amount of regulator immediately available at the active sites. 



{Hi) The 'intrinsic activity (McRae, Foster, and Bonner, 1953), defined in 

 relation to the number of regulator molecules bound to the active sites, and 

 thus indicating the specific growth activity of these molecules when properly 

 situated (or of the receptor-regulator complex). Apparently the 'intrinsic 

 activity is synonymous with the 'capacity' as used by Veldstra (1953) and by 

 Jonsson (1955). 



In a system previously devoid of auxin, or with a low degree of auxin 

 saturation, a regulator of the intermediate type can apparently be expected 

 to give positive auxin effects. In a system already saturated, or nearly so, 

 with auxin molecules of high intrinsic activity, it must on the other hand be able 

 to replace so many of these that the sum of intrinsic activities decreases, that 

 is, a competitive anti-auxin effect will occur. 



Substances which behave in this way are already known. As a good 

 example we will mention 4-methyl-phenoxyacetic acid (4-MePOA) (Aberg, 

 1954). It strikingly increases the growth of 2:4-D-inhibited flax roots, but on 

 the other hand, its own inhibiting effects may be effectively counteracted by 

 an anti-auxin like 1-NMSP. In the Avena cyhnder test it gives a peculiar 

 action curve {Figure 1), an initial inhibition being followed by a growth 

 restoration which, however, does not reach the control level before the ulti- 

 mate non-specific toxicity sets in. In the wheat root test an action curve of 

 the inverse type is obtained, while the fiax roots with their higher auxin 

 sensitivity and lower response to anti-auxins give a simple curve of the 'auxin 

 type'. The ultimate inhibition of the wheat roots may possibly be of complex 

 nature, auxin effects being mixed with non-specific toxicity. 



Curves similar to that of 4-MePOA have been found in the Avena cylinder 

 test for 1-naphthoxyacetic acid and 2-naphthoxy/jobutyric acid (Aberg and 

 Khahl, 1953), for 2-naphthylacetic acid, 2:6-dichlorophenoxyacetic acid, 

 3-methyl-phenoxyacetic acid, etc. Other substances, e.g. 2-methylphenoxy- 

 acetic acid and 2-naphthoxyacetic acid, give curves where the initial inhibi- 

 tion is followed by a stimulation up to nearly twice that of the control growth. 

 The action curve of phenoxyacetic acid also seems to belong to this main 



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