Abstract
Noninfectious bud-failure (BF) remains a major threat to almond production in California, particularly with the recent rapid expansion of acreage and as more intensive cultural practices and modern cultivars are adopted. BF has been shown to be inherited in both vegetative and sexual progeny, with exhibition related to the age and propagation history of scion clonal sources. These characteristics suggest an epigenetic influence, such as the loss of juvenility mediated by DNA-(de)methylation. Various degrees of BF have been reported among cultivars as well as within sources of clonal propagation of the same cultivar. Genome-wide methylation profiles for different clones within almond genotypes were developed to examine their association with BF levels and association with the chronological time from initial propagation. The degree of BF exhibition was found to be associated with DNA-(de)methylation and clonal age, which suggests that epigenetic changes associated with ageing may be involved in the differential exhibition of BF within and among almond clones. Research is needed to investigate the potential of DNA-(de)methylation status as a predictor for BF as well as for effective strategies to improve clonal selection against age related deterioration. This is the first report of an epigenetic-related disorder threatening a major tree crop.
Highlights
Previous research suggests that BF is a result of the failure of gene/gene complex expression required for normal winter dormancy and associated development of the vegetative bud[2]
Kester et al.[2] reported that BF-exhibition of twelve unique nursery sources was distinct in separation and dynamics patterns corresponding with the clonal age of the source, which suggests somaclonal variation not explained by DNA polymorphisms itself, presumably because the disorder is not associated with changes in the DNA sequence of the controlling gene(s), but rather involving the modification of gene activity through still poorly understood epigenetic-like mechanisms[19,20]
DNA-(de)methylation has been assessed in this material through Methylation profiles using methylation-sensitive amplified fragment length polymorphism (MS-AFLPs) in order to test for associations with increasing potential for BF-exhibition as well as ageing
Summary
Previous research suggests that BF is a result of the failure of gene/gene complex expression required for normal winter dormancy and associated development of the vegetative bud[2]. The presence and absence of methylation in the DNA [DNA-(de)methylation] affect clonal (mitotic) and seedling (meiotic) inheritance This phenomenon is associated with gene silencing during development and ageing in higher organisms, including the angiosperms[6]. Kester et al.[2] reported that BF-exhibition of twelve unique nursery sources was distinct in separation and dynamics patterns corresponding with the clonal age of the source, which suggests somaclonal variation not explained by DNA polymorphisms itself, presumably because the disorder is not associated with changes in the DNA sequence of the controlling gene(s), but rather involving the modification of gene activity through still poorly understood epigenetic-like mechanisms[19,20]. DNA-(de)methylation has been assessed in this material through Methylation profiles using methylation-sensitive amplified fragment length polymorphism (MS-AFLPs) in order to test for associations with increasing potential for BF-exhibition as well as ageing
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