Figure 1. The fast-freeze, deep-etch, rotary-shadowed replica technique is used to image cell wall architecture without the use of chemical fixatives and dehydrants. Pectins have been extracted from this onion parenchyma cell wall to expose the cellulose–xyloglucan network. One cellulose microfibril is drawn out. Cellulose microfibrils are paracrystalline arrays of several dozen (1 4)-d-glucan chains that tightly hydrogen bond to each other, both side-to-side and top-to-bottom. The arrangement of the glucan chains in a cross-section of a single microfibril, and the arrangement of atoms in the unit structure of the microfibril core, are shown. The glucan chains in the core of the microfibril have a precise spacing as determined by X-ray diffraction. (From R. J. Preston (1974) Physical Biology of the Plant Cell Wall, Chapman and Hall, London.) From studies involving solid-state nuclear magnetic resonance (NMR) spectroscopy, glucan chains at the surface of the microfibril are thought to adopt a slightly different alignment from 180°. (Courtesy of M. Jarvis)

Figure 2. The original multinet growth hypothesis explains that as walls stretch during growth, the microfibrils reorient passively from a transverse direction on the inner wall to a longitudinal direction at the outer wall. The hydrostatic pressure developed by the protoplasm is resisted by a relatively thin cell wall, and the tensile force pulling the microfibrils apart is several orders of magnitude higher than cell turgor pressure. For example, a spherical cell with a radius () of 50 m and 10 atm of turgor (P), enveloped by a cell wall only 0.1 m thick (t), develops 2500 atm of tension in the wall (₁). This enormous tension changes as the cell geometry changes. When this cell begins to elongate and become cylindrical, the tension increases to 5000 atm tangentially (₂) simply because of the change in cell dimension. Whereas the Slinky is difficult to pull outward because of the orientation of the coils, it is easily pulled longitudinally. Hence, cell shape is controlled in plants similarly. Altering the interaction between the tethering crosslinking glycans and cellulose is the principal determinant of cell expansion.

Figure 3. Wall loosening and incorporation of new wall polymers is integrated so that wall thickness is maintained during cell expansion. As the walls are only a few strata thick, loosening of the wall with no insertion of new wall material would very quickly thin the wall during growth and cause rupture. In contrast, deposition without loosening would increase wall thickness, because the walls would not expand.

Figure 4. Biosynthesis of the wall requires a coordination of the synthesis of cellulose microfibrils at the plasma membrane surface, with the synthesis and glycosylation of proteins and wall-modifying enzymes at the rough endoplasmic reticulum and the synthesis of all noncellulosic polysaccharides at the Golgi apparatus. Material destined for the cell wall is packaged into secretory vesicles, transported to the cell surface and integrated with the newly synthesized microfibrils. It is estimated that assembly of the new wall stratum begins when no more than 10 glucose residues of a cellulose chain are made.

Figure 5. Stress-relaxation is considered to be the underlying basis of cell expansion. When an elongating cell is stretched by turgor, the longitudinal stress is borne more or less equally by the glycans tethering the cellulose microfibrils. If some of the tethers are dislodged from the microfibrils or hydrolysed, then they temporarily ‘relax’ and the yield threshold is breached because the other tethers are strained. Water uptake results in expansion of the microfibrils, which attach to the relaxed glycans, and they again are placed under tensile stress. Microfibril separation driven by osmotic pressure of the cell is facilitated by loosening of the crosslinking glycans that tether them. This may be accomplished by coordinate action of expansins, which break the steric interactions between the crosslinking glycans and cellulose, and xyloglucan endotransglycosylase (XET), which hydrolyses a glycan and reattaches one part of the chain to the nonreducing terminus of another. This action by XET may also function in forming new tethers as microfibrils from inner lamellae merge with microfibrils of the outermost lamellae as they are pulled apart during wall extension.