Schaller A, Oecking C
Institute of Plant Sciences, ETH-Zürich, Universitätstrasse 2, CH-8092 Zürich, Switzerland.
Plant Cell. 1999 Feb;11(2):263-72. doi: 10.1105/tpc.11.2.263.
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.
系统素是番茄植株伤口诱导防御基因激活的重要介质，它能引起秘鲁番茄培养细胞生长培养基的快速碱化。通过调节质膜H⁺-ATP酶活性，研究了质膜质子通量与防御基因诱导之间可能的机制联系。发现H⁺-ATP酶抑制剂（赤藓红B、己烯雌酚和钒酸盐）可使秘鲁番茄细胞培养物的生长培养基碱化，并诱导整株番茄植株中的伤口反应基因。相反，H⁺-ATP酶激活剂（壳梭孢菌素）使秘鲁番茄细胞培养物的生长培养基酸化，并抑制系统素诱导的培养基碱化。同样，在经壳梭孢菌素处理的番茄植株中，发现伤口和系统素触发的伤口反应性mRNA积累受到抑制。然而，壳梭孢菌素处理番茄植株导致水杨酸积累和病程相关基因的表达。显然，伤口和病原体防御信号通路受质膜质子电化学梯度变化的差异调节。此外，发现秘鲁番茄细胞培养基的碱化依赖于Ca²⁺的流入和一种蛋白激酶的活性。还表明可逆蛋白磷酸化参与伤口反应基因的诱导。讨论了质膜H⁺-ATP酶作为Ca²⁺激活蛋白激酶的可能靶点及其在防御信号传导中的作用。
