<i>Arabidopsis</i> H⁺-ATPase AHA1 controls slow wave potential duration and wound-response jasmonate pathway activation.

Abstract

Electrogenic proton pumps have been implicated in the generation of slow wave potentials (SWPs), damage-induced membrane depolarizations that activate the jasmonate (JA) defense pathway in leaves distal to wounds. However, no defined H⁺-ATPases have been shown to modulate these electrical signals. Pilot experiments revealed that the proton pump activator fusicoccin attenuated SWP duration in <i>Arabidopsis</i> Using mutant analyses, we identified <i>Arabidopsis</i> H⁺-ATPase 1 (AHA1) as a SWP regulator. The duration of the repolarization phase was strongly extended in reduced function <i>aha1</i> mutants. Moreover, the duration of SWP repolarization was shortened in the presence of a gain-of-function <i>AHA1</i> allele. We employed aphid electrodes to probe the effects of the <i>aha1</i> mutation on wound-stimulated electrical activity in the phloem. Relative to the wild type, the <i>aha1-7</i> mutant increased the duration and reduced the amplitudes of electrical signals in sieve tube cells. In addition to affecting electrical signaling, expression of the JA pathway marker gene <i>JAZ10</i> in leaves distal to wounds was enhanced in <i>aha1-7</i> Consistent with this, levels of wound-response jasmonoyl-isoleucine were enhanced in the mutant, as was defense against a lepidopteran herbivore. The work identifies a discrete member of the P-type ATPase superfamily with a role in leaf-to-leaf electrical signaling and plant defense.