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First published online January 11, 2008; 10.1104/pp.107.112979 Plant Physiology 146:1040-1052 (2008) © 2008 American Society of Plant Biologists OPEN ACCESS ARTICLE
Bitterness in Almonds1,[C],[OA]Plant Biochemistry Laboratory, Department of Plant Biology, Center for Molecular Plant Physiology (R.S.-P, K.J., B.L.M.), and Chemistry Department (C.E.O.), Faculty of Life Sciences, University of Copenhagen, DK–1871 Frederiksberg C, Copenhagen, Denmark; and Departamento de Mejora Vegetal, Centro de Edafología y Biología Aplicada del Segura-Consejo Superior de Investigaciones Científicas, E–30100 Murcia, Spain (F.D.)
Bitterness in almond (Prunus dulcis) is determined by the content of the cyanogenic diglucoside amygdalin. The ability to synthesize and degrade prunasin and amygdalin in the almond kernel was studied throughout the growth season using four different genotypes for bitterness. Liquid chromatography-mass spectrometry analyses showed a specific developmentally dependent accumulation of prunasin in the tegument of the bitter genotype. The prunasin level decreased concomitant with the initiation of amygdalin accumulation in the cotyledons of the bitter genotype. By administration of radiolabeled phenylalanine, the tegument was identified as a specific site of synthesis of prunasin in all four genotypes. A major difference between sweet and bitter genotypes was observed upon staining of thin sections of teguments and cotyledons for β-glucosidase activity using Fast Blue BB salt. In the sweet genotype, the inner epidermis in the tegument facing the nucellus was rich in cytoplasmic and vacuolar localized β-glucosidase activity, whereas in the bitter cultivar, the β-glucosidase activity in this cell layer was low. These combined data show that in the bitter genotype, prunasin synthesized in the tegument is transported into the cotyledon via the transfer cells and converted into amygdalin in the developing almond seed, whereas in the sweet genotype, amygdalin formation is prevented because the prunasin is degraded upon passage of the β-glucosidase-rich cell layer in the inner epidermis of the tegument. The prunasin turnover may offer a buffer supply of ammonia, aspartic acid, and asparagine enabling the plants to balance the supply of nitrogen to the developing cotyledons.
1 This work was supported by the Danish National Research Foundation (to the Center for Molecular Plant Physiology) and the Spanish Ministry of Education and Science, including a postdoctoral fellowship (to R.S.-P.). The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Birger Lindberg Møller (blm{at}life.ku.dk). [C] Some figures in this article are displayed in color online but in black and white in the print edition. [OA] Open Access articles can be viewed online without a subscription. www.plantphysiol.org/cgi/doi/10.1104/pp.107.112979 * Corresponding author; e-mail blm{at}life.ku.dk. Received November 13, 2007; accepted December 29, 2007; published January 11, 2008. This article has been cited by other articles:
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