Abstract
The postulation proposed by Reed and his colleagues (11, 12) that the mode of action of Alar was through hydrolysis of the growth retardant to unsymmetrical dimethylhydrazine, UDMH, which subsequently inhibits diamine oxidase from converting tryptamine to indoleacetaldehyde, was examined. In vitro tests showed that commercial proteolytic enzyme preparations as well as those prepared from Alar-sensitive plants were not capable of breaking the C-N (peptide) bond in Alar. Both UDMH and β-hydroxyethylhydrazine (BOH) reacted, with indoleacetaldehyde to yield several compounds which gave positive spot tests for indole and hydrazine. Likewise, UDMH reacted readily with constituents in the endosperm-nucellar tissues when injected into immature almond ovules. Experiments with Alar, UDMH and BOH showed that Alar was more effective as a growth retardant and as a promotor of floral initiation than the others at nearly equal molar concentrations. Injections of Alar and 2-14C mevalonic acid, together and separately, into immature peach ovules revealed that the synthesis of kauren-19-ol, a gibberellic acid precursor, was depressed in the presence of Alar. None of these results support the hypotheses that 1) the active portion of Alar is the UDMH moiety and 2) the primary effect of Alar is to inhibit IAA synthesis.

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