Abstract
The phytohormone auxin is a major regulator of diverse aspects of plant growth and development. The ubiquitin-ligase complex SCF(TIR1/AFB) (for Skp1-Cul1-F-box protein), which includes the TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX (TIR1/AFB) auxin receptor family, has recently been demonstrated to be critical for auxin-mediated transcriptional regulation. Early-phase auxin-induced hypocotyl elongation, on the other hand, has long been explained by the acid-growth theory, for which proton extrusion by the plasma membrane H(+)-ATPase is a functional prerequisite. However, the mechanism by which auxin mediates H(+)-ATPase activation has yet to be elucidated. Here, we present direct evidence for H(+)-ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H(+)-ATPase and increased H(+)-ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H(+)-ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H(+)-ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, α-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H(+)-ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H(+)-ATPase phosphorylation. Our results define the activation mechanism of H(+)-ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
Highlights
The phytohormone auxin is a major regulator of diverse aspects of plant growth and development
Decapitated hypocotyl sections containing the elongating region were obtained from 3-d-old etiolated seedlings (Gendreau et al, 1997) and were stored on agar-solidified growth medium until a sufficient amount was gathered for analysis (Supplemental Fig. S1A)
The hypocotyl sections continued to elongate on the growth medium in the presence of the exogenous natural auxin indole-3acetic acid (IAA), hypocotyl elongation in the absence of indole-3-acetic acid (IAA) ceased within 30 min after excision (Supplemental Fig. S1B), as described previously (Christian and Lüthen, 2000)
Summary
The phytohormone auxin is a major regulator of diverse aspects of plant growth and development. Early-phase auxin-induced hypocotyl elongation, on the other hand, has long been explained by the acid-growth theory, for which proton extrusion by the plasma membrane H+-ATPase is a functional prerequisite. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H+-ATPase and increased H+-ATPase activity without altering the amount of the enzyme. The electrochemical potential gradient of protons across the plasma membrane that is created by the H+-ATPase provides the driving force for K+ uptake through inward-rectifying K+ channels (Claussen et al, 1997; Philippar et al, 2006) and subsequent water uptake These processes permit cell expansion, leading to elongation growth (Katou and Okamoto, 1992; Cosgrove, 2000; Hager, 2003). We postulated that H+-ATPase is activated by this phosphorylation system during earlyphase auxin-induced hypocotyl elongation
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
