Bitterness inheritance in apricot (P. armeniaca L.) seeds

Abstract

Seed bitterness, due to cyanogenic glucosides, has been reported in apricot as a recessive trait, being determined by a single gene. In this study, 21 F1 and 10 F2 populations from parents with either bitter or non-bitter ('sweet') phenotype were tested by seed tasting. Both the 'bitter' and the 'sweet' phenotypes were represented in populations from 'bitter×bitter' and 'sweet×sweet' crosses, as well as from self-pollination of either bitter-or sweet-seeded trees, providing evidence that more than one gene is involved in this trait. Ten populations showed segregation ratios inconsistent with a monofactorial inheritance of seed taste with the 'sweet' trait dominant over the 'bitter'. On the other hand, data from spectrophotometric assays indicate that seed cyanoglucoside content cannot be regarded as a quantitative trait. All the observed segregation ratios can be explained by an inheritance mechanism based on five, non-linked genes, involved in two distinct biochemical pathways. Three genes would control different steps in an 'additive' pathway (either the biosynthesis of cyanoglucosides, or their transport, or both) leading to accumulation of these metabolites in seeds:homozygosis of recessive alleles of at least one of them would result in the sweet phenotype. Two more genes would provide a cleaving activity, participating to cyanoglucoside catabolism; heterozygosis or homozygosis of dominant alleles at these loci would produce the 'sweet' phenotype, while homozygosis for recessive alleles of at least one of them would interrupt the catabolic pathway, leading to the 'bitter' trait, if associated with the anabolic function.

Accumulation Pattern of Amygdalin and Prunasin and Its Correlation with Fruit and Kernel Agronomic Characteristics during Apricot (Prunus armeniaca L.) Kernel Development

“…The two compounds are synthesized de novo in almond seeds, and the amygdalin content is significantly higher by 200- to 1000-fold in mature bitter almond seeds than in slightly bitter or sweet seeds [ 66 ]; our results were in accord with these observations. In apricot, amygdalin concentrations of 4400 to 6500 mg/100 g DW [ 72 ] or 5500 to 7000 mg/100 g DW [ 8 , 73 , 74 , 75 , 76 , 77 ] have been reported; our results also fall within this range. Cyanogenic glycosides occur naturally in many plants including apricot kernels, which contain up to 6% amygdalin and are the food most likely to cause acute cyanide toxicity.…”

Insights into research on phytochemistry and biological activities of Prunus armeniaca L. (apricot)

“…These compounds also give a bitter taste to apricot seeds of bitter phenotype (P. armeniaca var. amara) (Negri, Bassi, Magnanini, Rizzo, & Bartolozzi, 2008). However, consumption of the seeds containing cyanogenic glucosides may cause some degree of intoxication primarily on nervous system and thyroid.…”

Molecular markers for kernel bitterness in almond

“…Recent inheritance studies have provided evidence that more than one gene is involved in bitterness in other Prunus species such as apricot (Prunus armeniaca), where five unlinked genes involved in two distinct biochemical pathways (three in the biosynthesis of cyanoglucosides or their transport and two involved in the breakdown of cyanoglucosides) have been associated with bitterness (Negri et al 2008). In contrast, genetic studies in peach (Prunus persica) have proposed a monofactorial inheritance, with bitterness dominant to sweetness in kernels (Werner and Creller 1997).…”