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Articles

BREEDING FOR RESISTANCE TO ASPERGILLUS FLAVUS IN ALMOND

Article number
373_14
Pages
111 – 118
Language
Abstract
Aspergillus flavus Link, although only a weak pathogen of almond (Prunus dulcis (Mill.) D.A. Webb.), can contaminate susceptible nuts with mycotoxins.
Aflatoxins B1 and B2 have been detected in California almond samples at very low frequencies.
Single contaminated kernels may contain high levels of toxin, however.
The almond genetic improvement program at Davis, California is pursuing resistance to Aspergillus through the breeding for barriers to infection and colonization in the shell (endocarp), the seed coat and seed cotyledon.
Cultivar differences in the rate of colonization and sporulation of aflatoxigenic Aspergillus flavus on both intact and wounded seed were observed in a selection of almond cultivars grown in California.
Genotypes demonstrating barriers to fungal development in the intact seed coat as well as seed cotyledon tissue were identified.
The seed coat barrier was expressed as the absence of fungal colonization for up to 3 days following the inoculation of intact seed and was observed to be uniformly high for most cultivars tested.
Cotyledon resistance, which was expressed as a lower rate of fungal colonization and sporulation was identified only in the cultivars ‘Ne Plus Ultra’, ‘Ruby’ and ‘Carion’.

Kernel damage, particularly by the navel orangeworm Amyelois transitella (Walker) is frequently associated with Aspergillus infection of nuts.
The seed coat offers little protection from navel orangeworm.
Susceptibility appears to be dependent upon the integrity of shell seal rather than overall shell thickness or hardness.
While completely sealed shells show resistance to the navel orangeworm, the presence of only very small endocarp fractures may increase worm survival by providing a more protected environment for early larval development.

Publication
Authors
T.M. Gradziel, D.E. Kester
Keywords
aflatoxin, Prunus dulcis
Full text
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