Theories of Auxin Action 1 85 



wall pressure around the cell and would permit water uptake due to 

 this simple drop in turgor pressure. By this concept, growth is attrib- 

 uted to a dynamic function of the cell wall, as contrasted to the 

 dynamic function of the cytoplasm per se. The concept has been 

 criticized by Commoner and Mazia (1942) who demonstrated that ap- 

 parently flaccid cells would still take up water in response to auxin. 

 The stand that cell grov/th is primarily a function of the cell 

 wall has been supported further by the work of Burstrom (1953). 

 After a critical study of water uptake, as mentioned in the previous 

 section, he concluded that the cell wall attains a plastic quality dur- 

 ing growth, and that water uptake only follows the changes in the 

 wall. As evidence for this he cited the finding that root cells which 

 are at the appropriate stage for elongation attain a plastic quality in 

 the walls. Ihis plasticity can be observed whether the cells are per- 

 mitted to enlarge and take up water or whether they are essentially 

 prexenied from growing by immersion in hypertonic solutions. If the 

 wall plasticity is the primary action of growth, then cells should be 

 strictly unable to grow in isotonic or hypertonic solutions. Some care- 

 ful experiments on this aspect indicate that neither wheat root nor 

 Jerusalem artichoke cells may grow in such osmotic conditions (Bur- 

 strom, 1953). By his concept, then, the effects of auxin and respira- 

 tion upon growth are attained primarily through an activation of 

 cell wall growth. The wall is thought to be made plastic enough for 

 cell extension, and then the active deposition of new wall material 

 causes cell enlargement. The cytoplasm must be capable of taking up 

 enough water osmotically to keep up with the growing wall or else 

 growth will cease, as it apparently does in hypertonic solutions. 



TOXIC METABOLISM 



There is reason to believe that the inhibitory or toxic effects of 

 auxins may be physiologically distinct from the growth promoting 

 effects (cf. Burstrom, 1951). If the promotive effects and the toxic 

 effects are truly distinct, then the mechanism of the toxic actions of 

 auxins may be sought in functions other than those thought to be 

 responsible for growth. 



From a survey of root inhibition effects of various phenoxyacetic 

 acid derivatives, Leaper and Bishop (1950) have found that the most 

 inhibitory materials are ones in which two positions para to one an- 

 other on the ring are left unsubstituted. They point out that it would 

 not be difficult for two such positions to become oxidized to cjuinonoid 

 structures. Ouinones in general are, of course, highly toxic. If phenoxy- 

 acetic acids are converted into quinones as Leaper and Bishop sug- 



