Abscisic Acid Suppresses Hypocotyl Elongation by Dephosphorylating Plasma Membrane H+-ATPase in Arabidopsis thaliana

Plasma membrane H+-ATPase is thought to mediate hypocotyl elongation, which is induced by the phytohormone auxin through the phosphorylation of the penultimate threonine of H+-ATPase. However, regulation of the H+-ATPase during hypocotyl elongation by other signals has not been elucidated. Hypocotyl elongation in etiolated seedlings of Arabidopsis thaliana was suppressed by the H+-ATPase inhibitors vanadate and erythrosine B, and was significantly reduced in aha2-5, which is a knockout mutant of the major H+-ATPase isoform in etiolated seedlings. Application of the phytohormone ABA to etiolated seedlings suppressed hypocotyl elongation within 30 min at the half-inhibitory concentration (4.2 mu M), and induced dephosphorylation of the penultimate threonine of H+-ATPase without affecting the amount of H+-ATPase. Interestingly, an ABA-insensitive mutant, abi1-1, did not show ABA inhibition of hypocotyl elongation or ABA-induced dephosphorylation of H+-ATPase. This indicates that ABI1, which is an early ABA signaling component through the ABA receptor PYR/PYL/RCARs (pyrabactin resistance/pyrabactin resistance 1-like/regulatory component of ABA receptor), is involved in these responses. In addition, we found that the fungal toxin fusiccocin (FC), an H+-ATPase activator, induced hypocotyl elongation and phosphorylation of the penultimate threonine of H+-ATPase, and that FC-induced hypocotyl elongation and phosphorylation of H+-ATPase were significantly suppressed by ABA. Taken together, these results indicate that ABA has an antagonistic effect on hypocotyl elongation through, at least in part, dephosphorylation of H+-ATPase in etiolated seedlings.