Roles of water stress and phytotoxins in the development of Pierce's disease of the grapevine

Abstract

The water relations of healthy grapevines (Vitis vinifera cv. “Chardonnay”) were compared to those of nearby grapevines infected with the Pierce's disease (PD) bacterium under vineyard conditions. Xylem blockage in the node and petiole was associated with the development of marginal leaf chlorosis and necrosis for diseased vines. Diseased leaves developed a lower midday water potential (ψw) and lower cell turgor than healthy leaves. At midday, turgor of the chlorotic tissue of a diseased leaf decreased to near zero which was related to an increase in leaf solute potential (ψs). At dawn, leaf ψw and turgor were higher than at midday for both healthy and diseased leaves, but they remained significantly lower in diseased leaves. An increase in midday stomatal resistance was also associated with marginal leaf chlorosis and necrosis for grapevines with PD as well as for almond trees with almond leaf scorch, another disease caused by the PD bacterium. Diseased grape leaves had higher levels of proline than healthy leaves or symptomless leaves on diseased vines. Symptomless leaves on diseased vines also had distinctly less xylem blockage in the node and petiole, and lower midday stomatal resistance than leaves with PD symptoms. The biophysical and biochemical changes observed for diseased vines indicate that marginal leaf necrosis occurs when water stress develops. Diseased leaves are apparently water stressed because of vascular dysfunction which, when prolonged, may result in accelerated leaf senescence. The role of phytotoxin(s) in the development of PD was also investigated. The involvement of toxin(s) was questionable because sterile culture medium components caused leaf scorching similar to that previously attributed to toxin(s) produced by the PD bacterium. These medium components were present in both inoculated and noninoculated crude filtrates, and they were of similar low molecular weights as the reported phytotoxin(s).