Does indoleacetic acid promote growth via cell wall acidification?

Planta ◽  
1978 ◽  
Vol 140 (2) ◽  
pp. 137-142 ◽  
Author(s):  
David G. Pope
1998 ◽  
Vol 118 (2) ◽  
pp. 557-564 ◽  
Author(s):  
Christopher P. Keller ◽  
Elizabeth Van Volkenburgh

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Matyáš Fendrych ◽  
Jeffrey Leung ◽  
Jiří Friml

Despite being composed of immobile cells, plants reorient along directional stimuli. The hormone auxin is redistributed in stimulated organs leading to differential growth and bending. Auxin application triggers rapid cell wall acidification and elongation of aerial organs of plants, but the molecular players mediating these effects are still controversial. Here we use genetically-encoded pH and auxin signaling sensors, pharmacological and genetic manipulations available for Arabidopsis etiolated hypocotyls to clarify how auxin is perceived and the downstream growth executed. We show that auxin-induced acidification occurs by local activation of H+-ATPases, which in the context of gravity response is restricted to the lower organ side. This auxin-stimulated acidification and growth require TIR1/AFB-Aux/IAA nuclear auxin perception. In addition, auxin-induced gene transcription and specifically SAUR proteins are crucial downstream mediators of this growth. Our study provides strong experimental support for the acid growth theory and clarified the contribution of the upstream auxin perception mechanisms.


1997 ◽  
Vol 100 (3) ◽  
pp. 415-422 ◽  
Author(s):  
Winfried S. Peters ◽  
Christa Lommel ◽  
Hubert Felle

1969 ◽  
Vol 17 (2) ◽  
pp. 229 ◽  
Author(s):  
AB Wardrop

In Eryngium vesiculosum and E. rostratum, the leaf collenchyma is characterized by the development of a lignified secondary wall in the final stages of cell differentiation. The collenchyma wall is rich in pectic substances which are distributed uniformly. In the outer limiting region of the collenchyma wall the microfibril orientation is random and this structure is considered to be the wall formed at cell division. The collenchyma wall consists of six to eight layers in which the microfibrils are alternately transversely and longitudinally oriented. Each layer consists of a number of lamellae of microfibrils. In the secondary lignified wall the cellulose microfibrils are arranged helically, the direction of their orientation making an angle of 40-45° to the cell axis. Excised leaf segments showed greatest elongation in solutions of glucose and 3-indoleacetic acid, when the collenchyma walls were thin, and no elongation occurred in segments in which secondary wall formation had commenced. In radial sections layers of transversely oriented microfibrils could not be seen distant from the lumen although discontinuities in wall texture were apparent. Layers of transversely oriented microfibrils could be seen adjacent to the lumen. It is suggested that reorientation of layers of initially transversely oriented microfibrils takes place during elongation of the cells.


2021 ◽  
Author(s):  
Zhenbiao Yang ◽  
Wenwei Lin ◽  
Wenxin Tang ◽  
Koji Takahashi ◽  
Hong Ren ◽  
...  

Abstract The phytohormone auxin controls a myriad of processes in plants, at least in part through its regulation of cell expansion. The "acid growth hypothesis" has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism underlying auxin-induced cell wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane (PM) H+-ATPase that pumps protons into the apoplast, yet how auxin activates its phosphorylation remains elusive. Here, we show that the transmembrane kinase (TMK) auxin signaling proteins interact with PM H+-ATPases and activate their phosphorylation to promote cell wall acidification and hypocotyl cell elongation in Arabidopsis. Auxin induced TMK's interaction with H+-ATPase on the plasma membrane within 1-2 minutes as well as TMK-dependent phosphorylation of the penultimate Thr residue. Genetic, biochemical, and molecular evidence demonstrates that TMKs are required for auxin-induced PM H+-ATPase activation, apoplastic acidification, and cell expansion. Thus, our findings reveal a crucial connection between auxin and PM H+-ATPase activation in regulating apoplastic pH changes and cell expansion via TMK-based cell surface auxin signaling.


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