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

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

2021
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Overview
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. Auxin induces transmembrane-kinase-dependent activation of H + -ATPase in the plasma membrane through phosphorylation of its penultimate threonine residue, promoting apoplastic acidification and hypocotyl cell elongation in Arabidopsis .