Plant Defense Response to Fungal Pathogens (Activation of Host-Plasma Membrane H+-ATPase by Elicitor-Induced Enzyme Dephosphorylation)

Abstract

Extensive research in the last few years has disclosed a sequence of biochemical events that appear to participate in activation of plant disease defense reactions. Early in the interaction between the plant host and the pathogen, signals are produced that induce responses in the respective partners. This process involves the interaction between pathogenassociated molecules (elicitors) and putative plant receptors. This recognition is followed by a signal transduction cascade resulting in defense gene activation and the expression of disease resistance in the plant host. Specific recognition between the plant host and the fungal pathogen determines the outcome of the interaction (Keen, 1990). The resistance or susceptibility of host plants to different races of a fungal pathogen is determined by the match of dominant resistance genes in the plant with dominant avirulence genes (avr genes) in the pathogen (De Wit, 1992). The avr genes, in at least a few well-studied systems, have been shown to code directly or indirectly for elicitor molecules; resistance genes are suggested to code directly or indirectly for receptor molecules (De Wit, 1992).

Blue light activates the plasma membrane H+-ATPase by phosphorylation of the C-terminus in stomatal guard cells

“…Fungal pathogen-induced dephosphorylation of H ϩ -ATPase in vivo in cultured tomato cells (Vera-Estrella et al, 1994;Xing et al, 1996) and alkaline phosphatasemediated dephosphorylation of H ϩ -ATPase in vitro in tobacco cells (Desbrosses et al, 1998) result in an increase of H ϩ -ATPase activity. Systemin, a primary wounding signal, is suggested to inhibit H ϩ -ATPase activity via Ca 2ϩ -dependent phosphorylation of H ϩ -ATPase in cultured tomato cells (Schaller and Oecking, 1999).…”

“…Very similar results were obtained by in vivo treatment of intact tissue with the fungal toxin fusicoccin (FC), an activator of the H ϩ -ATPase, and it is suggested that FC induces a displacement of the C-terminal autoinhibitory domain of H ϩ -ATPase from its catalytic site (Palmgren, 1991;Johansson et al, 1993;Rasi-Caldogno et al, 1993). Such displacement of the C-terminus may be achieved by phosphorylation and dephosphorylation with physiological stimuli, and the C-terminus can be a substrate for protein kinase and protein phosphatase in vivo and in vitro (Schaller and Sussman, 1988;Serrano, 1989;Palmgren, 1991;Suzuki et al, 1992;Sekler et al, 1994;Vera-Estrella et al, 1994;Xing et al, 1996;Camoni et al, 1998;Sze et al, 1999).…”

Resistance gene-dependent plant defense responses.

“…These increases were accompanied by the concurrent acidification of the extracellular medium, which was caused by an increase in plasma membrane H+-ATPase activity (Vera-Estrella et al, 1994a). Slightly later (1 to 3 hr onward), specifically induced events included increased lipid peroxidation, elevated extracellular peroxidase activity, and the accumulation of extracellular phenolics.…”

The sink-specific and stress-regulated Arabidopsis STP4 gene: enhanced expression of a gene encoding a monosaccharide transporter by wounding, elicitors, and pathogen challenge.

“…In fact, studies by Hancock (1969Hancock ( , 1970 clearly showed that the uptake of 3-O-methylglucose (3-OMG) into hypocotyl sections from wounded or infected squash is higher than it is in control sections, and this additional transport activity was assigned to an inducible transporter in diseased or wounded hypocotyls. The energy that is necessary for this additional transport could be provided by elicitor-induced dephosphorylation and activation of the respective H+-ATPase (Vera-Estrella et al, 1994).…”