Skip to main content
ARS Home » Pacific West Area » Parlier, California » San Joaquin Valley Agricultural Sciences Center » Crop Diseases, Pests and Genetics Research » Research » Publications at this Location » Publication #292178
Title: Characterization of Xylella fastidiosa popP gene required for pathogenicity

Author
item SHI, XIANGYANG - University Of California
item TIAN, LI - University Of California
item Lin, Hong

Submitted to: American Phytopathological Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 4/15/2013
Publication Date: 8/10/2013
Citation: Shi, X., Tian, L., Lin, H. 2013. Characterization of Xylella fastidiosa popP gene required for pathogenicity. American Phytopathological Society Abstracts. 103:S2.132.

Interpretive Summary:

Technical Abstract: Xylella fastidiosa (Xf) possesses the two component regulatory system (TCS) popP/Q which differentially regulates genes in response to environmental stimuli. To elucidate the role of popP in Pierce’s disease of grapes, a site-directed deletion method and chromosome-based genetic complementation strategy were employed to create the Xf'popP mutant and complementary Xf'popP-C strains. Greenhouse-grown Cabernet Sauvignon grapes were mechanically inoculated with Xf'popP, Xf'popP-C and wild-type Xf Temecula. Three months after inoculation, no symptoms were observed in grapes inoculated with Xf'popP. However, grapevines inoculated with wild type Xf and Xf'popP-C showed a typical PD symptom. Xf titers in the grapevines inoculated with Xf'popP were significantly lower than that of Xf'popP-C and wild-type as estimated by quantitative PCR. In vitro studies showed that while the mutants and wild types had similar growth curves, Xf'popP appeared to have significantly reduced abilities to aggregate and adhere to the wall of culture tubes. Biofim production of Xf'popP was 42% less than that of wild type and Xf'popP-C. In vitro gene expression profile analyses of Xf'popP, Xf'popP-C, and wild type have been carried out to further investigate regulatory pathways of TCS popP/Q in response to Xf infection.