Consequences of administration of indoleacetic acid 



If the oxidase activity increases as cells age, at least two major questions 

 may be asked : {a) which of the two functional moieties of the enzyme 

 manifest the increase in activity, and (b) by what mechanism is the increase 

 in activity accomplished ? 



The answer to the first question seems to have been obtained by Dr. Pilet 

 in the root oi^ Lens cidinaris (Pilet and Galston, 1955). He has found that the 

 peroxide-generating capacity of the tissue closely parallels its lAA-oxidase 

 activity, rising as the cells age {Figures 8 and 9). Peroxidase activity, on the 

 other hand, shows no such increase, and may actually show a decline with 

 age of the cell [Figure 10). Furthermore, the addition of the peroxigenic 

 cofactor DCP raises peroxide genesis and lAA oxidase activity of the 

 meristematic region tremendously, but has little or no effect on the older 

 regions {Figure 11). This leads us to the conclusion that auxin destruction 

 is normally limited by the peroxide-generating capacity of the tissue, which 

 in turn is controlled by some naturally-occurring DCP-like substance. 

 The mode of action of DCP is, as I have indicated, open to several interpre- 

 tations (Siegel and Galston, 1955; Lockhart, 1955), but this subject cannot 

 be further discussed here. 



As for the second question, regarding the mechanism by which lAA 

 oxidase activity is increased in older cells, the answer appears to be that this 

 is somehow controlled by the lAA itself. We have found that if the young 

 tissues, low in lAA-oxidase activity, are pretreated with physiological 

 concentrations of lAA, then their capacity for lAA destruction increases 

 (Galston and Dalberg, 1954). This phenomenon appears to be a case of 

 induced enzyme formation, similar to those frequently described for micro- 

 organisms. Maximal induction results from the administration of ca. 10~' M 

 lAA, a concentration which is certainly in the physiological range for stems 

 though a little high for roots. Synthetic analogues of lAA, as well as certain 

 compounds of the anti-auxin type, are capable of inducing greater lAA- 

 oxidase activity, though they are not themselves substrates for the oxidase. 

 This again resembles the situation in certain micro-organisms, where 

 inductive activity has been demonstrated for molecules known not to be 

 attacked by the induced enzyme. 



The significance of the auxin-induced formation of an lAA-destroying 

 system can only be conjectured about, but certain attractive possibilities 

 present themselves. It seems possible that the decreased sensitivity to auxin 

 of older cells is a consequence of their higher lAA oxidase activity, which in 

 turn is a consequence of prior induction by lAA. According to this scheme, 

 the administration of lAA to a young cell not only initiates growth, but also 

 sets in motion a chain of events leading to the diminution and eventual 

 culmination of growth. This, if true, is a neat example of the 'feed-back' 

 required in all cybernetic systems. As I shall point out later, such an increased 

 oxidase level may also be of morphogenetic significance for the cell. 



The concept of the induced formation of an I AA-destroying system under 

 certain auxin levels, and its possible 'de-inductive' disappearance under 

 lower levels of auxin, permits the formulation of hypotheses to explain 

 endogenous rhythms of auxin, lateral bud inhibition, and certain types of 

 auxin interactions (Galston and Dalberg, 1954). These will not be further 

 discussed here. 



V 227 



