Mechanics of Auxin-induced Groxvth 323 



Experiments of this type have shown that lAA-induced cell wall 

 plasticization takes place even though the section is not elongating. 

 This plasticization is, however, of a special kind in that it is made and 

 stored in an amount which is proportional to the length of time dur- 

 ing which the tissue is treated with auxin. This relation is shown in 

 Figure 10. A brief auxin pretreatment makes it possible for a speci- 

 fied amount of auxin-induced residual growth to take place in the 

 second phase of the experiment. Twice as long an auxin pretreatment 

 permits twice as much residual growth. Clearly, the action of lAA is 

 not to bring about a general decrease in wall rigidity but rather to 

 change the wall in such a manner that it can yield by a specified 

 amount. 



Further characteristics of auxin-induced wall softening include the 

 facts that the process is aerobic, inhibited by varied respiratory inhib- 

 itors, and suppressed by ethionine. The act of elongation itself, on 

 the contrary, is not inhibited by anaerobiosis and is relatively less 

 sensitive to metabolic inhibitors. 



ROLE OF RESPIRATION 



It has been known for many years that the application of auxins, 

 including lAA to plant tissue, including Avena coleoptile sections, 

 results in rapid and considerable increases in respiratory rate (Bon- 

 ner, 4, 6). It has been natural, therefore, to seek an understanding of 

 auxin-induced growth in terms of the respiratory response. It ap- 

 pears, however, that such search is fruitless. lAA-induced increase in 

 respiratory rate, in the Avena coleoptile at least, does not accompany 

 lAA-induced cell wall softening in nonelongating sections (0.3M 

 mannitol) (Ordin et aL, 20). The respiratory increase which accom- 

 panies lAA-induced growth is therefore an artifact of extension rather 

 than a direct effect of lAA. It is also clear, however, that lAA-induced 

 cell wall softening requires respiratory energy, supplied perhaps in the 

 form of ATP since the phosphorylative uncoupling agent, 2,4-dini- 

 trophenol, blocks lAA action. 



INTERACTION OF CELL WALL AND CYTOPLASM 



Since the ultimate effect of lAA treatment is upon the cell wall 

 and since lAA-induced cell wall softening requires the participation 

 of mitochondrial respiration, it is perhaps obvious that wall and 

 cytoplasm interact in auxin-induced growth. It is nonetheless of in- 

 terest that auxin-induced cell wall softening does not occur in plas- 

 molyzed sections in which cytoplasm and wall are in only tenuous 

 contact (Cleland, 10). Such sections are not injured by the treatment 

 since they respond to lAA upon deplasmolysis. 



