scholarly journals The Acid Growth Theory of auxin-induced cell elongation is alive and well.

1992 ◽  
Vol 99 (4) ◽  
pp. 1271-1274 ◽  
Author(s):  
D L Rayle ◽  
R E Cleland

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.



Planta ◽  
1985 ◽  
Vol 163 (4) ◽  
pp. 494-499 ◽  
Author(s):  
U. Kutschera ◽  
P. Schopfer


1990 ◽  
Vol 93 (3) ◽  
pp. 931-939 ◽  
Author(s):  
Hartwig Lüthen ◽  
Michael Bigdon ◽  
Michael Böttger


1981 ◽  
Vol 68 (3) ◽  
pp. 664-667 ◽  
Author(s):  
S. Ann Dreyer ◽  
Virginia Seymour ◽  
Robert E. Cleland




2020 ◽  
Vol 71 (1) ◽  
pp. 379-402 ◽  
Author(s):  
Minmin Du ◽  
Edgar P. Spalding ◽  
William M. Gray

The promotive effect of auxin on shoot cell expansion provided the bioassay used to isolate this central plant hormone nearly a century ago. While the mechanisms underlying auxin perception and signaling to regulate transcription have largely been elucidated, how auxin controls cell expansion is only now attaining molecular-level definition. The good news is that the decades-old acid growth theory invoking plasma membrane H+-ATPase activation is still useful. The better news is that a mechanistic framework has emerged, wherein Small Auxin Up RNA (SAUR) proteins regulate protein phosphatases to control H+-ATPase activity. In this review, we focus on rapid auxin effects, their relationship to H+-ATPase activation and other transporters, and dependence on TIR1/AFB signaling. We also discuss how some observations, such as near-instantaneous effects on ion transport and root growth, do not fit into a single, comprehensive explanation of how auxin controls cell expansion, and where more research is warranted.



2021 ◽  
Vol 22 (5) ◽  
pp. 2317
Author(s):  
Małgorzata Polak ◽  
Waldemar Karcz

Two arguments against the “acid growth theory” of auxin-induced growth were re-examined. First, the lack of a correlation between the IAA-induced growth and medium acidification, which is mainly due to the cuticle, which is a barrier for proton diffusion. Second, acid- and the IAA-induced growth are additive processes, which means that acid and the IAA act via different mechanisms. Here, growth, medium pH, and membrane potential (in some experiments) were simultaneously measured using non-abraded and non-peeled segments but with the incubation medium having access to their lumen. Using such an approach significantly enhances both the IAA-induced growth and proton extrusion (similar to that of abraded segments). Staining the cuticle on the outer and inner epidermis of the coleoptile segments showed that the cuticle architecture differs on both sides of the segments. The dose-response curves for the IAA-induced growth and proton extrusion were bell-shaped with the maximum at 10−4 M over 10 h. The kinetics of the IAA-induced hyperpolarisation was similar to that of the rapid phase of the IAA-induced growth. It is also proposed that the K+/H+ co-transporters are involved in acid-induced growth and that the combined effect of the K+ channels and K+/ H+ co-transporters is responsible for the IAA-induced growth. These findings support the “acid growth theory” of auxin action.



Planta ◽  
1985 ◽  
Vol 163 (4) ◽  
pp. 483-493 ◽  
Author(s):  
U. Kutschera ◽  
P. Schopfer


Planta ◽  
1991 ◽  
Vol 186 (1) ◽  
Author(s):  
RobertE. Cleland ◽  
Graham Buckley ◽  
Sogol Nowbar ◽  
NinaM. Lew ◽  
Charles Stinemetz ◽  
...  


2020 ◽  
Vol 71 (10) ◽  
pp. 2982-2994 ◽  
Author(s):  
Xiaoran Xin ◽  
Lei Lei ◽  
Yunzhen Zheng ◽  
Tian Zhang ◽  
Sai Venkatesh Pingali ◽  
...  

Abstract Auxin-induced cell elongation relies in part on the acidification of the cell wall, a process known as acid growth that presumably triggers expansin-mediated wall loosening via altered interactions between cellulose microfibrils. Cellulose microfibrils are a major determinant for anisotropic growth and they provide the scaffold for cell wall assembly. Little is known about how acid growth depends on cell wall architecture. To explore the relationship between acid growth-mediated cell elongation and plant cell wall architecture, two mutants (jia1-1 and csi1-3) that are defective in cellulose biosynthesis and cellulose microfibril organization were analyzed. The study revealed that cell elongation is dependent on CSI1-mediated cell wall architecture but not on the overall crystalline cellulose content. We observed a correlation between loss of crossed-polylamellate walls and loss of auxin- and fusicoccin-induced cell growth in csi1-3. Furthermore, induced loss of crossed-polylamellate walls via disruption of cortical microtubules mimics the effect of csi1 in acid growth. We hypothesize that CSI1- and microtubule-dependent crossed-polylamellate walls are required for acid growth in Arabidopsis hypocotyls.



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