4.1 Article

Effects of GA3+4 and GA4+7 Application Either Alone or Combined with Prohexadione-Ca on Fruit Development of Japanese Pear 'Kosui'

期刊

HORTICULTURE JOURNAL
卷 85, 期 3, 页码 201-208

出版社

JAPAN SOC HORTICULTURAL SCI
DOI: 10.2503/hortj.MI-107

关键词

bioactive GA; GA biosynthesis; gibberellin; fruit maturation; Pyrus pyrifolia (Burm.) Nakai

资金

  1. Grants-in-Aid for Scientific Research [16H04874] Funding Source: KAKEN

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In order to promote increases in the size of 'Kosui' Japanese pear [Pyrus pyrifolia (Burm.) Nakai] fruit by plant growth regulators, we applied gibberellin (GA)(3+4) paste [2.7% (w/w), A(3):A(4) = 90:10] in combination with prohexadione-calcium [1%, PCa; BAS-125 (3-oxido-4-propionyl-5-oxo-3-cyclohexene-carboxylate)], an inhibitor of GA 2 beta-hydroxylation that catabolizes active GA into an inactive form, to fruit pedicels at approximately 30 days after full bloom. GA(3+4)+PCa treatment advanced fruit growth only in the early stages, but fruit weight did not show any significant differences between the untreated control and GA(3+4)+PCa-treated fruits at harvest. In contrast, when GA(4+7) [2.7% (w/w), A(4):A(7) = 66:34] was applied, the fruit weight at harvest was greater than that of untreated fruit. Moreover, GA(4+7) treatment in combination with PCa resulted in an even higher fruit weight at harvest. The GA(4) concentration in fruit flesh was not affected by GA(3+4) application at 1 week after the treatment (WAT) either with or without PCa, but GA(4) levels increased with GA(4+7)+PCa treatment, resulting in a significant increase in fruit weight at harvest. A single GA(4+7) application almost doubled the GA(4) concentration compared with the untreated control, but the difference was not significant. These results indicate that fruit weight at harvest was greater when the GA(4) concentration was higher in the fruit flesh at 1 WAT. The higher concentration of GA(4) in the GA(4+7)+PCa-treated fruit compared with the GA(4+7) treatment alone may be attributed to the function of PCa that acts to prevent the inactivation of GA(4) to GA(34) by inhibiting 2 beta-hydroxylation.

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