The phytohormone auxin controls many processes in plants, at least in part through its regulation of cell expansion1. The acid growth hypothesis has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism that underlies auxin-induced cell-wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane H+-ATPase that pumps protons into the apoplast2, yet how auxin activates its phosphorylation remains unclear. Here we show that the transmembrane kinase (TMK) auxin-signalling proteins interact with plasma membrane H+-ATPases, inducing their phosphorylation, and thereby promoting cell-wall acidification and hypocotyl cell elongation in Arabidopsis. Auxin induced interactions between TMKs and H+-ATPases in the plasma membrane within seconds, as well as TMK-dependent phosphorylation of the penultimate threonine residue on the H+-ATPases. Our genetic, biochemical and molecular evidence demonstrates that TMKs directly phosphorylate plasma membrane H+-ATPase and are required for auxin-induced H+-ATPase activation, apoplastic acidification and cell expansion. Thus, our findings reveal a crucial connection between auxin and plasma membrane H+-ATPase activation in regulating apoplastic pH changes and cell expansion through TMK-based cell surface auxin signalling.
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Acknowledgemacents We thank the members of the Yang laboratory for discussion and comments on this work; J. Leung (Department of Institute Jean-Pierre Bourgin, INRA) for ost2-2D seeds; K. Iba (Kyushu University) for 35S::GFP-AHA1 seeds; C. Grefen (University of Tubingen) for FRET analyses 2in1 binary vectors; and L. Shan (University of Texas A&M) for protoplast transient expression vectors. This work was in part supported by an NIH grant (GM100130) to Z.Y.; K.T. (20K06685) and T.K. (20H05687 and 20H05910) were funded by MEXT/ JSPS KAKENHI. W.M.G. was funded by NIH (GM067203). H.Z. was funded by NIH (S10OD016400).
© 2021, The Author(s).
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't