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

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.