Growth, Enzyme and Sugar Responses of Immature Sugarcane to Foliar Treatment with 6-Azauracil and Gibberellic Acid

How to Cite

Alexander, A. G. (1968). Growth, Enzyme and Sugar Responses of Immature Sugarcane to Foliar Treatment with 6-Azauracil and Gibberellic Acid. The Journal of Agriculture of the University of Puerto Rico, 52(4), 295–310.


Immature sugarcane grown by sand culture was treated with foliar sprays of 6-azauracil, and 6-azauracil combined with gibberellic acid (GA). There were four objectives: 1, To verify growth-inhibitory effects of azauracil and to define the lowest effective concentration; 2, to determine whether growth inhibition can be maintained in the presence of a powerful growth stimulus; 3, to determine the influence of azauracil on protein and sugar constituents of treated plants; and 4, to determine whether inhibitor action can be correlated with activity of essential hydrolytic and oxidative enzymes. One experiment was conducted with seven concentrations of foliar azauracil. A second experiment combined three inhibitor concentrations with three levels of GA. All plants were treated once at 14 weeks of age and a single harvest was made 6 weeks later. Results are summarized as follows: 1. Azauracil injury symptoms appeared within 72 hours among plants given the highest inhibitor level (0.40 percent), and within 8 days for plants receiving as little as 0.005 percent. Severe symptoms included general yellowing of the foliage with localized red to red-brown spots on leaves. Similar spots plus parallel red streaks appeared on sheaths. A solid band of darkened tissue was often visible immediately below the dewlap. Death of tissues occurred at leaf tips and margins. Newly emerging leaves were yellowed, malformed, and apparently nonfunctional. Tillers were also malformed. Symptoms remained throughout the study. 2. Plants treated with 0.40-percent azauracil were dead within 15 to 20 days. Meristematic tissues died in those given 0.10 percent, but otherwise the plants survived in a stunted condition. The lowest inhibitor level causing significant growth decline was 0.04 percent. 3. Sucrose accumulated in immature storage tissue in response to increasing azauracil. As little as 0.01 percent caused a major sucrose rise, and 0.04 percent yielded about fourfold increases. Azauracil caused a general loss of fructose, suggesting a suppression of invertase. 4. Each of the enzymes assayed declined sharply with increasing inhibitor concentration. These included acid phosphatase, ATP-ase, amylase, in vertase, polyphenol oxidase, and peroxidase. Based on activity trends from plants surviving the inhibitor treatment, the tissues are believed to have been almost totally deficient of enzyme activity at the time of death. The inhibitor effect was far more pronounced in immature storage tissues than in leaves. This suggests a rapid translocation from leaves to storage areas and possible accumulation in tissue having intense biochemical activity. 5. Water-soluble protein was increased up to threefold by 6-azauracil in immature storage tissue. A similar but less pronounced effect was found in leaves. 6. Combination of 6-azauracil with GA generally verified growth, sugar, enzyme, and protein effects observed earlier. Growth inhibition was retained at all GA levels. High GA, equivalent to 0.10 percent of the pure acid, partially countered an azauracil suppression of fresh weight, millable stalk weight and internode length. Meristematic tissues were killed by high azauracil, 0.05 percent, but remained alive when high GA was combined with the inhibitor. 7. Evidence suggests that combined azauracil and GA promoted physiological maturity more effectively than either agent acting alone. S. Gibberellic acid generally increased sugar content and retarded enzyme action as a main effect. 9. Brix and polarization values were raised both by GA and 6-azauracil as main effects. Combination of 0.01-percent GA with 0.05-percent azauracil gave the maximum brix and polarization values recorded. 10. Possible mode of action of 6-azauracil in cane is discussed from the standpoint of disrupted nucleic acid synthesis. It is suggested that the precise information needed for synthesis of discrete enzymes is uncoded from nucleic acid carriers, with subsequent deficiency of catalytic potential following in proportion to inhibitor level. Biochemical consequences of hydrolytic and oxidative enzyme deficiency in cane are pointed out.


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