120 L. J. Audus and ]. K. Bakhsh 



could certainly be explained on a basis of heightened lAA-oxidase 

 content which, like that in the lAA-adapted roots, appears to be 

 greater in the meristematic end of the segment. Furthermore the 

 very close similarities in the curves of cell growth distribution shown 

 by TIBA- and lAA-adapted segments raise the question whether 

 they might not have similar underlying causes linked with the high 

 induced lAA-oxidase activity. It could be suggested that under these 

 conditions endogenous auxin concentration is lowered far below 

 the supraoptimal levels supposed to exist in roots and that the 

 marked difference in growth at the two ends is a reflection of differ- 

 ences in lAA concentration maintained by the oxidase at the two 

 ends. At the basal end it is near optimal, accounting therefore for 

 the apparently real stimulation of extension over the corresponding 

 cells of normal segments. At the apical end it is markedly suboptimal, 

 giving much reduced growth. But if this were so, one would have 

 expected applied lAA, even though most of it were oxidized, to 

 have given at least some slight stimulation of extension in this apical 

 region. Since there is no sign of this, the lower growth cannot be due 

 to lAA deficiency. As previously suggested for lAA adaptation, it 

 might more probably be due to the more rapid accumulation there 

 of a staling product from lAA oxidation in the apical cells. 



Segments From Roots Grown in DCA (10^ g/ml) 



Nine identical factorial experiments have tested the sensitivity of 

 DCA-grown segments to lAA concentrations of 5 X 10"^ '^^'^ 10 ^ 

 g/ml. From the mean segment extension data of Figure 4A it will 

 be seen that DCA-grown segments extend in sucrose only about half 

 as much as normal segments. But examination of Figures 4B and C 

 will show that adapted cells are not so restricted in their extension 

 as these figures would suggest. The reason for this discrepancy is 

 that roots grown in this DCA concentration have shorter meristems 

 and segments thus contain fewer cells, many more of which have al- 

 ready started to extend at the time of excision. The over-all exten- 

 sion of these segments is therefore correspondingly smaller. There 

 is no indication here that this growth limitation is restricted to any 

 part of the segment, and, as with 2,4-D, it is most rational to explain 

 this uniformly reduced growth as a result of the direct inhibiting 

 action of residual DCA retained adsorbed at the growth centers. On 

 grounds of molecular structure one might expect the rings to show 

 similar affinities for the growth centers. 



The action of lAA is to produce only slight reduction of adapted 

 segment growth, amounting to 11 per cent at 10 ' g/ml. Although this 

 is significant over the whole set of experiments, in the particular 



