The Role of Auxin in Cell Wall Expansion

Abstract

Plant cells are surrounded by cell walls, which are dynamic structures displaying a strictly regulated balance between rigidity and flexibility. Walls are fairly rigid to provide support and protection, but also extensible, to allow cell growth, which is triggered by a high intracellular turgor pressure. Wall properties regulate the differential growth of the cell, resulting in a diversity of cell sizes and shapes. The plant hormone auxin is well known to stimulate cell elongation via increasing wall extensibility. Auxin participates in the regulation of cell wall properties by inducing wall loosening. Here, we review what is known on cell wall property regulation by auxin. We focus particularly on the auxin role during cell expansion linked directly to cell wall modifications. We also analyze downstream targets of transcriptional auxin signaling, which are related to the cell wall and could be linked to acid growth and the action of wall-loosening proteins. All together, this update elucidates the connection between hormonal signaling and cell wall synthesis and deposition.

Keywords: acid growth; auxin; cell expansion; cell wall.

Figure 1

The role of auxin in cell wall expansion. Isodiametric plant cell preparing for elongation (A), undergoing elongation (B) and fully elongated (C). The cell contains intracellular structures such as nucleus (n) and vacuole(s) (v) in the cytosol (c) and is surrounded by plasma membrane (PM). Outside of the PM the cell wall (CW) is present (A–C). The PM consists of a phospholipid bilayer (in blue), while the cell wall consists of different polysaccharides such as cellulose microfibrils (CMFs in yellow), pectins (green double line), XyGs (red line) and other polysaccharides (not shown). Auxin activates plasma membrane H⁺-ATPase proton pumps, which pump protons (H⁺) into the wall matrix, leading to wall acidification (a). Acidification of the apoplast activates potassium channels, which transport potassium ions (K⁺) to the cytosol, stimulating water (H₂O) uptake and maintaining tensile stress (yellow arrows in A and B) (b). Acidic pH activates wall-loosening proteins and enzymes, which loosen the connections between different cell wall polysaccharides (c). PMEs activate plasma membrane nicotinamide adenine dinucleotide phosphate (NADPH), transporting superoxide anions to the cell wall where they are converted to hydrogen peroxide (d). Wall-loosening proteins and enzymes cause CMF sliding and moving apart, which increases wall porosity (e). Cell wall extension leads to the activation of calcium channels and calcium efflux into the cytosol (f). Accumulation of cytosolic calcium inhibits H⁺-ATPase proton pumps and protoplast alkalization (g). Newly synthesized polysaccharides are inserted into the wall, where they arrive via vesicular trafficking (h). Wall alkalization activates PMEs, which in turn activate wall-degrading enzymes (i) and NADPH (j) causing crosslinking of the wall polysaccharides and growth cessation (k).