Ascorbic acid as an effective antioxidant in apple to alleviate browning molecular studies of control of the biosynthesis

Apple fruit are subject to multiple stressors during pre- and post-harvest development that can cause an increase in detrimental reactive oxygen species (ROS). In addition, many cultivars are prone to postharvest storage disorders such as internal browning and soft scald that may result from ROS accumulation. To determine the role AsA plays in maintenance of apple fruit integrity, a baseline was established using apples that are standard in the industry, 'Delicious, ' 'Golden Delicious' and 'Fuji.' There was more AsA in peel than cortex for all cultivars during on-tree development and in storage. The quantity declined as ripening progressed. AsA was highest in, and at later stages localized to, the core line and vascular bundles of the fruit. To determine the role of AsA in the development of soft scald in 'Honeycrisp' apples, the amount was quantified via HPLC and RT-PCR for the enzymes involved in the AsA recycling pathway was performed. AsA was higher in peel than cortex at all time points. The results showed a complex AsA recycling cycle, indicating it may play some role in preventing soft scald. The role AsA plays in Braeburn browning disorder was examined comparing 'Braeburn' and 'Gala' AsA levels in CA storage that was inducing to browning. AsA does not seem to play a role in the prevention of browning, as levels were higher in brown cortex tissue from 'Braeburn' than healthy cortex in 'Gala.' To determine what mechanisms control BBD, two suppressive subtractive hybridization libraries were constructed. Healthy cortex displayed stress related and cell maintenance genes, whereas brown cortex had no stress response genes. 'A lack of properly functioning pathways, rather than a specific gene causing browning, may be involved in the development of browning

Sequence‐Based Introgression Mapping Identifies Candidate White Mold Tolerance Genes in Common Bean

Core Ideas Sequenced‐based introgression mapping rapidly maps QTL to a physical location A highly polymorphic candidate gene associated with apoptosis maps in the WM7.1 QTL A highly polymorphic gene associated with effector recognition maps in the WM8.3 QTL White mold, caused by the necrotrophic fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a major disease of common bean (Phaseolus vulgaris L.). WM7.1 and WM8.3 are two quantitative trait loci (QTL) with major effects on tolerance to the pathogen. Advanced backcross populations segregating individually for either of the two QTL, and a recombinant inbred (RI) population segregating for both QTL were used to fine map and confirm the genetic location of the QTL. The QTL intervals were physically mapped using the reference common bean genome sequence, and the physical intervals for each QTL were further confirmed by sequence‐based introgression mapping. Using whole‐genome sequence data from susceptible and tolerant DNA pools, introgressed regions were identified as those with significantly higher numbers of single‐nucleotide polymorphisms (SNPs) relative to the whole genome. By combining the QTL and SNP data, WM7.1 was located to a 660‐kb region that contained 41 gene models on the proximal end of chromosome Pv07, while the WM8.3 introgression was narrowed to a 1.36‐Mb region containing 70 gene models. The most polymorphic candidate gene in the WM7.1 region encodes a BEACH‐domain protein associated with apoptosis. Within the WM8.3 interval, a receptor‐like protein with the potential to recognize pathogen effectors was the most polymorphic gene. The use of gene and sequence‐based mapping identified two candidate genes whose putative functions are consistent with the current model of Sclerotinia pathogenicity