Redox and wall-restructuring

Diverse mechanisms contribute to primary cell wall re-structuring, causing wall loosening and tightening (increasing and decreasing extensibility, respectively). Wall loosening can occur by enzymic hydrolysis and possibly also elimination-degradation of polysaccharides; by enzymic transglycosylation of xyloglucan; by expansin-mediated rupture of hemicellulose–cellulose tethers; and by non-protein-mediated scission of polysaccharides through hydroxyl radical attack. Tightening can occur by enzymic de-esterification of pectin enabling Ca2+-bridge formation; and by peroxidase-catalysed coupling of phenol–polysaccharide complexes and of tyrosine-containing glycoproteins. Several loosening and tightening mechanisms involve redox reactions; low-molecular-weight oxidants and anti-oxidants in the apoplast can therefore control wall extensibility. Apoplastic ascorbate is unusual in potentially being either an anti-oxidant or a pro-oxidant (the latter via Fenton reaction-mediated production of hydroxyl radicals). Many wall-localised reactions are known only from model experiments in vitro: an important future challenge is to explore the relative contributions of postulated reactions in the walls of living plant cells. To this end, a clear distinction is required between enzyme activity (assayed in vitro) and enzyme action (occurring in vivo).