|Doddapaneni,, Harsha - UC DAVIS|
|Fritschi,, Felix - UNIV OF MISSOURI|
|Walker,, M. Andrew - UC DAVIS|
Submitted to: National Viticulture Research Conference
Publication Type: Abstract Only
Publication Acceptance Date: May 30, 2008
Publication Date: June 7, 2008
Citation: Lin, H., Doddapaneni,, H., Fritschi,, F.B., Walker,, M. 2008. Characterization and identification of pd resistance mechanisms: analyses of xylem anatomical structures and molecular interactions of host/xylella fastidiosa. In: Proceedings of 2nd Annual Viticulture Research Conference, July 9-11,2008, Davis, California. p.46-47. Technical Abstract: The xylem-limited bacterium Xylella fastidiosa (Xf) causes Pierce’s disease (PD) with symptoms primarily due to xylem vessel blockage in susceptible grapevines. Virulence may be related to pathogen titer, presence or absence of chemical compounds in xylem sap, and/or anatomical features of the xylem. Experimental, as well as anecdotal, information indicates a considerable range in tolerance to PD exists among grapevine genotypes. It appears that a number of Vitis and Muscadinia species have evolved mechanisms that allow them to tolerate Xf infection. The goal of this study was to identify and characterize physiological, anatomical, biochemical and molecular events in the grape/Xf interaction between resistant and susceptible genotypes and among different tissue types. Our results have clearly shown differences in response of Vitis species to Xf infection. In general, resistant genotypes tend to have lower Xf cell counts in the xylem, even at late stages of disease development, and have fewer tyloses, compared to susceptible genotypes such as V. vinifera. Results of genome-wide transcriptional studies further support this differential response hypothesis and have identified putative genes, involving signal transduction and defense response pathways in response to Xf infection. Similarly, the xylem sap studies have shown that Xf response varies with the nature of xylem sap treatment and that such a response is linked to differential expression of virulence genes.