Articles
BITTERNESS IN ALMOND
Article number
1028_10
Pages
73 – 76
Language
English
Abstract
Although nowadays most of almond cultivars produce sweet almond kernels the original taste of almond kernel was bitter.
How and when the divergence between these genotypes occurred is still unknown.
Because most of the cultivated almonds already contain one bitter allele, new bitter almond seedlings are usually obtained in the cross breeding programs.
Therefore, it would be interesting to develop a molecular marker that enables the breeder to eliminate early the bitter seedlings in the nursery.
Breeding studies crossing sweet and bitter genotypes showed that bitterness is a monogenic recessive trait.
Its locus, Sweet kernel (Sk) locus, was localized in linkage group five (G5) in an almond genetic linkage map, although its biochemical function remains unknown.
Molecular marker studies identified four microsatellites as linked to and flanking the Sk/sk gene, that can be very useful for the selection of this character in almond breeding with an efficiency rate of 97%. However, a pre-study of the parents for each cross is needed.
In bitter almonds, hydrogen cyanide is produced upon hydrolysis of amygdalin following tissue disruption.
Amygdalin and its precursor prunasin are cyanogenic glucosides.
Amygdalin is mainly present in the kernels, whereas prunasin can be detected in the vegetative parts as well as in the fruit mother tissues.
Biochemical and cloning studies have shown some differences in the enzymes involved in the degradation pathway, called prunasin hydrolases.
Genome studies performed in two sweet and two bitter almond genotypes have shown more than 200 single nucleotide polymorphisms in a 3 Mb region in which Sk locus is included within G5. The elucidation of the polymorphisms defining bitterness will be decisive to identify the Sk gene and the development of a molecular marker for bitterness in almond.
How and when the divergence between these genotypes occurred is still unknown.
Because most of the cultivated almonds already contain one bitter allele, new bitter almond seedlings are usually obtained in the cross breeding programs.
Therefore, it would be interesting to develop a molecular marker that enables the breeder to eliminate early the bitter seedlings in the nursery.
Breeding studies crossing sweet and bitter genotypes showed that bitterness is a monogenic recessive trait.
Its locus, Sweet kernel (Sk) locus, was localized in linkage group five (G5) in an almond genetic linkage map, although its biochemical function remains unknown.
Molecular marker studies identified four microsatellites as linked to and flanking the Sk/sk gene, that can be very useful for the selection of this character in almond breeding with an efficiency rate of 97%. However, a pre-study of the parents for each cross is needed.
In bitter almonds, hydrogen cyanide is produced upon hydrolysis of amygdalin following tissue disruption.
Amygdalin and its precursor prunasin are cyanogenic glucosides.
Amygdalin is mainly present in the kernels, whereas prunasin can be detected in the vegetative parts as well as in the fruit mother tissues.
Biochemical and cloning studies have shown some differences in the enzymes involved in the degradation pathway, called prunasin hydrolases.
Genome studies performed in two sweet and two bitter almond genotypes have shown more than 200 single nucleotide polymorphisms in a 3 Mb region in which Sk locus is included within G5. The elucidation of the polymorphisms defining bitterness will be decisive to identify the Sk gene and the development of a molecular marker for bitterness in almond.
Authors
R. Sánchez-Pérez
Keywords
Prunus dulcis, breeding, bitterness, amygdalin, cyanogenic glucosides
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