Neio Theory on Primary Mode of Auxin Action 457 



lAA. That, of course, is very readily explained and doesn't differ in 

 principle from the antagonism system of Dr. Bonner and his school. 

 It is a cjuestion of materials competing for the same site. In the case 

 of lAA versus 2,4-D, you have 2,4-D sitting here and lAA can't get 

 in, and vice versa. So that is simply explained by this scheme of solu- 

 bilization adsorption in the cytoskeleton. The other point you men- 

 tioned regarding nitriles and methyl esters — they, of course, are 

 more fat soluble than the acids; therefore, they solubilize better into 

 the lipophilic cytoskeleton so they concentrate there and, therefore, 

 the chances of attaching to a specific auxin site are also increased. 

 The materials are probably hydrolized before they act as auxins 

 (Figure 3 A and B). 



Dr. Wain: There are quite a number of points I would like to 

 raise on this paper, but wish to deal with four. I want to point out that 

 with mono- and dichlorophenoxyacetic acids you get activity in a 

 number of cases. The 2,6-derivative is active, as has been demonstrated 

 by numerous workers; much less activity is shown by the 3,5-com- 

 pound; indeed, this substance is inactive in all our tests. With the 

 mono- and dimethylphenoxyacetic acids you have inactivity both 

 with the 3,5- and the 2,6-derivatives. Methyl derivatives, in general, 

 are less active than the corresponding chloro-compounds. A full paper 

 on the phenylacetic acids will appear shortly, but in the meantime here 

 are some results obtained in three tests (Table 1). You will observe 

 that phenylacetic acid itself is active, and so are all the chloro- 

 derivatives we examined. Now, the point I want you to notice here 

 is that there is particularly good activity in the 3-, the 2,3-, the 2,6-, 

 and the 2,3,6- derivatives. 



Bearing in mind what I've just said, I want to go back to Dr. 

 van Overbeek's diagram of phenoxyacetic acid with 2,6 blocking; the 

 molecule is sitting up there with the carboxyl group in the wrong 

 position for activity. If you have 3,5 blocking, the molecule will be 

 still further out of the so-called cytoskeleton. Dr. van Overbeek would 

 say, "That's exactly what I would expect because the compound is in- 

 active." But, in fact, if you make the 2,3,5- or the 3,4,5- compounds, 

 you restore activity; yet the compound is still presumably in the same 

 position as it was before. Secondly, we have the tetrachloro-deriva- 

 tives; the 2,3,4,5-compound, again 3,5 blocked, is quite active, as Dr. 

 Smith has shown. 



Dr. van Overbeek: Let me answer the easy question as to why the 

 methyl derivative is less active than the chloro compound: The methyl 

 group, being lighter in weight, even though it has the same bulk, 

 naturally sticks less rigidly to the cytoskeleton by van der Waals 

 force. Dr. R. Brian, at the Wye College conference, showed that the 

 behavior of the penetration of these auxin molecules into a mono- 



