The 2009 ASHS Annual Conference
2170:
Identification of the Chromosomal Genomic Regions Associated with Peach Tree Short Life Syndrome Using Microsatellite/SSR Markers
2170:
Identification of the Chromosomal Genomic Regions Associated with Peach Tree Short Life Syndrome Using Microsatellite/SSR Markers
Tuesday, July 28, 2009
Illinois/Missouri/Meramec (Millennium Hotel St. Louis)
Peach Tree Short Life (PTSL) is a complex disease syndrome involving nematodes, winter temperature, orchard history, pruning, Pseudomonas syringae and secondary pathogens. The disease occurs commonly in the southeastern U.S., and possibly in other areas of the U.S., Europe, South America and South Africa as the related Bacterial Canker Complex. PTSL causes premature tree death typically during the 2nd through 5th years after planting, resulting in large economic losses for growers. Recently, Guardian® BY520-9' rootstock was selected for its tolerance to PTSL; however, the genetic basis for this tolerance remains unknown. Nemaguard, a PTSL susceptible rootstock, and Guardian® selection 3-17-7 were crossed. Each F1 plant was selfed to create segregating F2 populations. One hundred and seventy microsatellite/simple sequence repeat (SSR) markers, each uniquely mapped to chromosomal locations on the Prunus reference genome, were used to screen the two parents and F1-11. Forty-seven SSR markers showed polymorphism among the parents and were heterozygous in F1-11. Segregation data obtained from the F2-11 population for SSR marker inheritance and their PTSL-response in a PTSL field trial were compiled to identify nuclear genomic regions associated with the response to PTSL. Of the 47 polymorphic SSRs, nine (distributed on 4 linkage groups) were genetically linked with the response to PTSL through Analysis of Variance (SAS). Identified SSR markers would be useful in marker-assisted selection to facilitate selection of PTSL-tolerant rootstocks. Using Joinmap® 3.0 software, a genetic map with seven linkage groups was constructed from 30 of the 47 polymorphic markers with coverage of 217.5 cM. QTL analysis was conducted using PLABQTL1.2 software by implementing the composite interval mapping method. QTLs were detected from 0 to 10 cM from the upper terminus of linkage group 2 in each of the five years evaluated. Two SSR markers located within the QTL were also found to be associated with the response to PTSL by individual marker analysis. The upper region of linkage group 2 appeared to be important because both the individual SSR analysis and the QTL analysis linked this region with the response to PTSL. The genes controlling tolerance or susceptibility to PTSL may reside in this region. In the future, developing more SSR or other high-resolution markers to saturate this region will further define the specific region, and ultimately identify the target genes.
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