Increases in the Capacity of Pea Tissue to Form Acyl‐aspartic Acids Specifically Induced by Auxins

S ummary A study has been made of the factors which influence the rate of formation of 3‐indoIeacetyl‐L‐aspartate and i‐naphthaleneacetyl‐L‐aspartate when segments of etiolated pea stems are treated with 3‐indolylacetic acid (IAA) and i‐naphthaleneacetic acid (NAA). When the tissue is placed in the auxin solution there is an initial lag in the formation of each conjugate and the maximal capacity is not reached until 6 hours. If the tissue is pretreated with non‐radioactive IAA or NAA for 8–14 hours before transference to radioactive IAA or NAA, the amount of conjugate formed in the next 2 hours is up to six times greater than that formed in tissues receiving no pretreatment. Apparent substrate saturation of the system is reached when the external concentration of IAA and NAA is about 50 and 15 mg/1 respectively. Induction of the formation of IAA aspartate is not a consequence of auxin‐induced extension growth since it also takes place in fully extended segments. The capacities of other auxins to induce the formation of both IAA and NAA aspartateswere assessed. It was established that both conjugates are also induced when the segments are pretreated with 2,4‐dichlorophenoxyacetic acid, 2,3,6‐trichlorobenzoic acid and S‐carboxymethyl‐N, N‐dimethyldithiocarbamate. In contrast, pretreatment with other carboxylic acids such as benzoic acid (which itself can form an aspartate) or transcinnamic acid, 3, 5‐dichlorophenoxy‐acetic acid and α‐2, 4‐dichlorophenoxy‐iso‐butyric acid does not affect the rate of formation of either IAA or NAA aspartate. These findings are interpreted in terms of induced enzyme formation in a system where the capacity for induction is specifically restricted to compounds which have a high auxinic activity. It is also clear that compounds showing a high inductive capacity are not necessarily suitable substrates nor are substrates necessarily capable of induction.