Summaira Riaz, M. Andrew Walker,* and Alan Tenscher
*UC Davis, Department of Viticulture and Enology, UC Davis, Davis, CA 95616 (awalker@ucdavis.edu)

A successful breeding program relies on sources of resistance from multiple, diverse backgrounds to develop resistant varieties. This lets breeders stack major and minor resistance loci through conventional breeding to ensure long-lasting resistance in the field.  In this study, we identified Pierce’s disease (PD) resistance in b42-26, a hybrid form of Vitis arizonica and V. girdiana obtained by Harold Olmo in Loreto in Baja, California. The F1 breeding population of 352 seedling plants was developed by crossing the susceptible V. vinifera (F2-35) with b42-26. A genetic map was developed with simple sequence repeat (SSR) markers. The level of polymorphism in b42-26 was very low, perhaps due to its isolation on the Baja California peninsula, which may have resulted in an inbred genetic background. The genetic map was developed with 191 SSR markers and grouped to 18 chromosomes. Chromosome 19 was not represented due to b42-26’s homozygosity, even though we tested the population with 45 SSR markers associated with that chromosome. All seedling plants were phenotyped for PD resistance in the greenhouse and data were analyzed with MAPQTL v. 6.0. The analysis located resistance on chromosome 8 and this was verified in the pBC1 and pBC2 populations. The resistance locus was named PdR2 and it resides between markers FAM82 and VMC 7h2. We are employing closely linked markers to allow the PD winegrape breeding program to stack the PdR1b and PdR2 loci together, thus broadening PD resistance.

We gratefully acknowledge research funding from the CDFA Pierce’s Disease Board

Funding Support: CDFA PD/GWSS Board