596 W. S. Hillman and W. K. Purves 



of Figure 2, which injured the previous hypotheses, are harmless here: 

 it would be reasonable to expect GA-induced elongation in the pres- 

 ence of inhibitory auxin levels if GA increased the other component 

 of the auxin reaction system rather than increasing or protecting 

 auxin itself. 



A major source of support for this general view can be found in 

 numerous reports of systems in which a response to GA is dependent 

 upon, or greatly increased by, the presence of exogenous auxin. The 

 most striking such system has been described by Kuse (6). GA-IAA 

 synergisms have also been found for the elongation of sections from 

 light-grown pea seedlings and in starved etiolated sections (2) al- 

 though in our work with etiolated pea sections the effects of GA and 

 lAA under all circumstances have been additive or subadditive. The 

 existence of GA-IAA synergisms, however, does not demonstrate an 

 auxin-mediated action of gibberellin; it may simply indicate that 

 such systems are so strongly auxin-depleted that auxin is absolutely 

 limiting to growth. It is notable that in some systems the action of 

 kinetin (6-furfurylaminopurine) is similarly dependent upon the pres- 

 ence of auxin, yet it has not been concluded that kinetin acts di- 

 rectly on auxin metabolism (13). Returning to oiu" own work, we 

 note that there is an almost absolute dependence of GA-induced (but 

 not of auxin-induced) elongation in SI sections on the presence of 

 sucrose. It would be unwise to conclude from this, however, that GA 

 action is specifically mediated by carbohydrate metabolism. Although 

 none of these conclusions can be rejected, they cannot be accepted 

 on this sort of evidence. 



It has been suggested (2) in support of auxin-mediated GA action 

 that the lower response of subapical older tissue to GA is due to its 

 lower auxin content. It is certainly evident that such tissue is auxin- 

 limited, since added auxin can increase its elongation. However, the 

 auxin occasions no increase in the GA response (Figure 1). Of course, 

 since the apical and subapical sections differ considerably anatomically, 

 it really is not to be expected that a single factor such as auxin would 

 account for the difference in GA response. 



11 GA acts directly to increase a nonauxin component of the 

 auxin reaction system, the relation between lAA- and GA-induced 

 elongation in our experiments is sinprisingly loose. Either previous 

 decapitation of the plants or inclusion of PCIB in the test medium re- 

 duces the control growth and at the same time results in an increased 

 response to lAA, thus creating a strong presumption of a change in 

 the auxin relations of the tissues. In effect, either treatment appears 

 to make auxin more limiting. Yet the elongation induced by GA re- 



