LINKING THE MODEL OF THE DEVELOPMENT OF PD IN GRAPEVINES TO AN UNDERSTANDING OF THE DYNAMICS OF GWSS TRANSMISSION OF X. FASTIDIOSA TO GRAPEVINES AND GRAPVINE GENE EXPRESSION MARKERS OF PD

Authors: LABAVITCH, JOHN - UC, DAVIS; Backus, Elaine; MATTHEWS, MARK - UC, DAVIS; SHACKEL, KEN - UC, DAVIS

Submitted to: CDFA Pierce's Disease Control Program Research Symposium
Publication Type: Proceedings
Publication Acceptance Date: 10/12/2006
Publication Date: 11/27/2006
Citation: Labavitch, J.M., Backus, E.A., Matthews, M., Shackel, K. 2006. Linking the model of the development of PD in grapevines to an understanding of the dynamics of GWSS transmission of X. fastidiosa to grapevines and grapvine gene expression markers of PD. CDFA Pierce's Disease Control Program Research Symposium Proceedings. p. 283.

Interpretive Summary: For several years we have been studying the development of Pierce’s Disease (PD) in grapevines. Our studies have been guided by a model of PD development that describes several steps in disease development following inoculation of Xylella fastidiosa (Xf), the bacterium that causes PD. Our hypotheses have proven accurate, although parts of the model are still being tested. We have shown that xylem vessel blockage and the following reductions in the ability of the stem to transport water are early consequences of infection with Xf. Ethylene treatment of vines also triggers vessel blockage and reduced water movement, and ethylene release from vines may increase following infection. We have also shown that Xf must pass through vessel pit membranes to spread systemically in the plant. This suggests that digestion of cell walls of the pit membranes is likely to be important. In this report, we describe our continuing studies indicating that Xf produces two cell wall-degrading enzymes that can open the pit membrane network, allowing the pathogen to spread throughout an infected grapevine.

Technical Abstract: For several years we have been studying the development of Pierce’s Disease (PD) in grapevines. Our studies have been guided by a model of PD development proposed with our initial application for funding. The Model proposed several steps in disease development following introduction of the PD causal agent, the bacterium Xylella fastidiosa (Xf): Xf introduction to vessels => vessel cavitation => initial water deficit => Xf population increase => production of enzymes by Xf =>cell wall digestion => oligosaccharide signals => ethylene synthesis rise => a wave of vessel occlusion beyond the infection site => collapse of vine water transport => leaf abscission => vine death. Our hypotheses have proven quite accurate, although aspects of the model are still being tested. We have shown that xylem vessel obstruction (tyloses, plant cell wall component-derived gels, and bacterial extracellular polysaccharides) and consequent reductions in stem water transport capacity are early consequences of infection with Xylella fastidiosa (Xf), before bacterial populations are substantial and have spread far from the inoculation point. We have shown that ethylene treatment of vines also triggers vessel obstruction and reduced water movement and that ethylene emanation from vines may increase following infection. We have also developed data for xylem vessel length distributions in grapevines and shown that Xf must pass through vessel pit membranes for the bacteria is to move systemically, thus suggesting that digestion of cell wall polymers in the pit membranes is likely to be important. We describe herein continuing studies indicating that Xf produces cell wall-degrading polygalacturonase (PG) and endo-'-1,4-glucanase (EGase) and that these two enzymes are sufficient to open the pit membrane network, allowing the pathogen to move systemically in infected grapevines.