Systemin is an important mediator of
wound-induced defense gene activation in tomato plants, and it elicits a rapid alkalinization of the growth medium of cultured Lycopersicon peruvianum cells. A possible mechanistic link between
proton fluxes across the plasma membrane and the induction of defense genes was investigated by modulating plasma membrane
H+-ATPase activity. Inhibitors of
H+-ATPase (
erythrosin B, diethyl
stilbestrol, and
vanadate) were found to alkalinize the growth medium of L. peruvianum cell cultures and to induce
wound response genes in whole tomato plants. Conversely, an activator of the
H+-ATPase (
fusicoccin) acidified the growth medium of L. peruvianum cell cultures and suppressed
systemin-induced medium alkalinization. Likewise, in
fusicoccin-treated tomato plants, the
wound- and
systemin-triggered accumulation of
wound-responsive mRNAs was found to be suppressed. However,
fusicoccin treatment of tomato plants led to the accumulation of
salicylic acid and the expression of pathogenesis-related genes. Apparently, the
wound and pathogen defense signaling pathways are differentially regulated by changes in the
proton electrochemical gradient across the plasma membrane. In addition, alkalinization of the L. peruvianum cell culture medium was found to depend on the influx of Ca2+ and the activity of a
protein kinase. Reversible
protein phosphorylation was also shown to be involved in the induction of
wound response genes. The plasma membrane
H+-ATPase as a possible target of a Ca2+-activated
protein kinase and its role in defense signaling are discussed.