TMK-based cell-surface auxin signalling activates cell-wall acidification

Article

关键词: MEMBRANE H+-ATPASE;    C-TERMINAL REGION;    PLASMA-MEMBRANE;    14-3-3 PROTEIN;    INDUCED PHOSPHORYLATION;    ELONGATION;    BINDING;    INHIBITION;    EXPRESSION;    MECHANISM;   

DOI  :  10.1038/s41586-021-03976-4

来源: SCIE

【 摘 要 】

The phytohormone auxin controls many processes in plants, at least in part through its regulation of cell expansion(1). 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 apoplast(2), 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.

【 授权许可】

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