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Published on January 11, 2008; 10.1104/pp.107.112979

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Received November 13, 2007
Accepted December 29, 2007

Bitterness in almonds (Prunus dulcis (Miller) D. A. Webb)

Raquel Sanchez Perez , Kirsten Jorgensen , Carl Erik Olsen , Federico Dicenta , and Birger Lindberg Moller *

Plant Biochemistry Laboratory, Department of Plant Biology, Center for Molecular Plant Physiology (PlaCe); Chemistry Department, Faculty of Life Sciences, University of Copenhagen, DK-1871 Frederiksberg C, Copenhagen, Denmark; Departamento de Mejora Vegetal, CEBAS-CSIC, PO Box 164, E-30100 Espinardo, Murcia, Spain

* Corresponding author; email: blm{at}life.ku.dk.

Bitterness in almond (Prunus dulcis (Miller) D. A. Webb) 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. LC-MS 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 radiolabelled 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 {beta}-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 {beta}-glucosidase activity, whereas in the bitter cultivar, the {beta}-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 {beta}-glucosidase rich cell layer in the inner epidermis of the tegument. The prunasin turn-over may offer a buffer supply of ammonia, aspartic acid, and asparagine enabling the plants to balance the supply of nitrogen to the developing cotyledons.




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