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 µM), 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.
Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya, 464-8602 Japan.
Yuki
Y
Hayashi
Koji
K
Takahashi
Shin-Ichiro
S
Inoue
Toshinori
T
Kinoshita
D000040:Abscisic Acid / Q000494:pharmacology*; D017360:Arabidopsis / Q000187:drug effects / Q000201:enzymology* / Q000254:growth & development*; D029681:Arabidopsis Proteins / Q000378:metabolism; D002462:Cell Membrane / Q000201:enzymology*; D064527:Etiolation / Q000187:drug effects; D006027:Glycosides / Q000494:pharmacology; D018546:Hypocotyl / Q000187:drug effects / Q000254:growth & development*; D008954:Models, Biological; D009154:Mutation / Q000235:genetics; D010766:Phosphorylation / Q000187:drug effects; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D006180:Proton-Translocating ATPases / Q000378:metabolism
D029681:Arabidopsis Proteins; D006027:Glycosides; C501210:KAT1 protein, Arabidopsis; D024661:Potassium Channels, Inwardly Rectifying; C007808:fusicoccin; D000040:Abscisic Acid; D006180:Proton-Translocating ATPases
Abscisic acid; Arabidopsis thaliana; Auxin; Dephosphorylation; Hypocotyl elongation; Plasma membrane H+-ATPase