Xylella fastidiosa Requires Polygalacturonase for Colonization and Pathogenicity in Vitis vinifera Grapevines

Abstract

Xylella fastidiosa is the causal agent of Pierce's disease of grape, an economically significant disease for the grape industry. X. fastidiosa systemically colonizes the xylem elements of grapevines and is able to breach the pit pore membranes separating xylem vessels by unknown mechanisms. We hypothesized that X. fastidiosa utilizes cell wall degrading enzymes to break down pit membranes, based on the presence of genes involved in plant cell wall degradation in the X. fastidiosa genome. These genes include several beta-1,4 endoglucanases, several xylanases, several xylosidases, and one polygalacturonase (PG). In this study, we demonstrated that the pglA gene encodes a functional PG. A mutant in pglA lost pathogenicity and was compromised in its ability to systemically colonize Vitis vinifera grapevines. The results indicate that PG is required for X. fastidiosa to successfully infect grapevines and is a critical virulence factor for X. fastidiosa pathogenesis in grapevine.

Genomic Insights into Xylella fastidiosa Interactions with Plant and Insect Hosts

“…Only the role of the polygalacturonase, encoded by pglA on the virulence of X. fastidiosa, has been addressed experimentally. Importantly, a pglA mutant exhibited greatly reduced ability to colonize grape and therefore incited very little symptom development (Roper et al 2007). While the mutant could be re-isolated from near the point of inoculation, it was severely restricted in its longdistance movement along the grape xylem vessels (Roper et al 2007).…”

“…Importantly, a pglA mutant exhibited greatly reduced ability to colonize grape and therefore incited very little symptom development (Roper et al 2007). While the mutant could be re-isolated from near the point of inoculation, it was severely restricted in its longdistance movement along the grape xylem vessels (Roper et al 2007). It seems likely that its greatly reduced motility is attributable to its inability to degrade pit membranes that serve to restrict both lateral and longitudinal movement of the pathogen between xylem vessels.…”

“…It therefore has been suggested that X. fastidiosa makes an EPS molecule similar to that of xanthan gum made by Xanthomonas campestris, but one which is lacking terminal mannosyl residues (Silva et al 2001). Antibodies that could recognize the EPS produced by X. fastidiosa were recently used to illustrate its production both in culture and in planta (Roper et al 2007). Generation of gum mutants (Killiny et al 2013) recently helped to better characterize the role of EPS in X. fastidiosa virulence.…”

A chitinase is required for Xylella fastidiosa colonization of its insect and plant hosts

“…These results suggest that ChiA contributes to vesselto-vessel movement of X. fastidiosa within plants, a process needed for dispersal through the plant and for disease symptom development [35]. To date, only pglA (encoding polygalacturonase A) has been shown to be important for X. fastidiosa movement among vessels, and consequently, symptom development [36]. While a pglA mutant was less virulent to grapevines than the wild-type control, it was recovered with high frequency and at populations only 10-fold lower than the wild-type strain at 37 cm above the inoculation site [36].…”

“…To date, only pglA (encoding polygalacturonase A) has been shown to be important for X. fastidiosa movement among vessels, and consequently, symptom development [36]. While a pglA mutant was less virulent to grapevines than the wild-type control, it was recovered with high frequency and at populations only 10-fold lower than the wild-type strain at 37 cm above the inoculation site [36]. This indicates that the pglA mutant was only moderately impaired in host colonization relative to that of the chiA mutant strain.…”