Pflra-substitution in regulators with phenyl nuclei 



is a very difficult one, and the solution will certainly depend on the attain- 

 ment of a better insight into the complex chain of processes connecting the 

 genotype of an organism with the result of its growth processes. Meanwhile 

 we may correlate empirically the action of the auxins with different growth 

 results. The fundamental outcome of such studies is that a substance showing 

 auxin activity in a certain growth process will probably do it also in other 

 connections (Went and Thimann, 1937; Audus, 1953), This could mean 

 that there is a common receptor, but the possibility of several receptors with a 

 similar affinity for different auxins must not be overlooked. It would also be 

 reasonable to expect some variations in the type of the receptor (or group of 

 receptors) for different plant species. In this connection well-documented 

 exceptions from the rule of coupled and general activity may be of considerable 

 interest. 



A typical competitive auxin antagonist, or anti-auxin, wovild now be a 

 substance which is bound to the auxin receptor in the same place as the 

 auxins, but which gives a complex unable to initiate the usual growth 

 responses. There is at present a rather extensive series of substances, for 

 example 1-naphthylmethylsulphideacetic acid and the corresponding 

 a-propionic acid (1-NMSA and 1-NMSP), a-(4-chlorophenoxy)-?^o-butyric 

 acid, l( — )-a-(2-naphthoxy)-«-butyric acid, 4-chloro/ra/2^cinnamic acid, and 

 4-z.5'o-propyl-phenoxyacetic acid, which may be assumed to behave in this 

 way. All substances mentioned above : (a) counteract the inhibiting effects 

 of externally applied auxin upon flax root growth, even if applied in con- 

 centrations which are without effect on or slightly depress the growth of 

 control roots, {b) stimulate the growth of intact flax roots slightly and that of 

 wheat roots strongly, the latter ones presumably containing a more highly 

 supra-optimal content of native auxin than do flax roots (cf. Aberg, 1955), 

 (c) inhibit the growth of Avena coleoptile sections. As far as tested, these 

 substances also counteract the effect of externally applied auxins on Avena 

 coleoptile sections in the manner expected (McRae and Bonner, 1953; 

 Aberg and KhaHl, 1953). Many other anti-auxins are known which are not 

 yet tested by all of the different methods, or which show slight deviations from 

 the pattern mentioned (e.g. no stimulation of flax roots). Such deviations 

 are natural with respect to the occurrence of various complications in the 

 physiological system (competition during uptake and transport, synergism, 

 effects upon auxin metabolism, non-specific toxicity). No alternative to the 

 hypothesis of a competitive auxin antagonism which is able to connect and 

 explain the growth phenomena mentioned above has as yet been proposed. 



The counteraction of the effects of externally applied auxins could 

 naturally be partly or wholly related to a hypothetical antagonism during the 

 uptake (see Aberg, 1953b). Owing to the exceedingly low concentrations 

 of the active substances which must be used, such a question is not easily 

 attacked by direct methods, and the possibility of surface effects complicates 

 the situation considerably. A comparison between the antagonistic effects 

 obtained in different tests may, however, give some clues. Preliminary 

 results for a series of homologous l-( — )-2-naphthoxy-alkylcarboxylic acids 

 do indicate that a 'bulky' substituent in the side chain of an anti-auxin 

 may possibly interfere to some extent with its uptake (gradually decreased 

 stimulation of wheat root growth, decreased inhibition of Avena cylinder 



95 



