Cartoon of primary cell wall structure and a working model of CW enzymes and proteins implicated in fruit softening. The ML is the layer between primary cell walls (PCW) of neighboring cells, which are external to the plasma membrane (PM). TCJs are a part of the ML, the places where 3 cells meet. One cellulose layer is depicted in this wall model. Xyloglucan binds to hydrophobic surfaces at cellulose–cellulose junctions to form a limited xyloglucan-cellulose (X-C) amalgam called biomechanical hotspots involved in CW loosening (extension/creep) (Park and Cosgrove 2012). EXP is a key protein agent that disrupts the xyloglucan-cellulose amalgam, and causes wall creep, while endo-1,4-β-glucanase (cellulase, Cel) and XTH may also act as wall loosening agents (Cosgrove 2016). Pectins, including HG, RGI, and RGII make extensive contacts with cellulose, and occupy the space between cellulose layers. HG is the most abundant pectin, particularly in the ML, and is deesterified by PME in blockwise or random demethylation patterns. Blockwise deesterified HG forms cross-links with Ca²⁺ to form an egg-box like pectate gel (shown in the ML and PCW), while random deesterified HG is degraded via endo-PG and PL, both actions have been detected during fruit ripening and postharvest storage. PL has a particular action on pectin in the TCJs, shown in pink in the MG fruit cartoon (top right). The PG β-subunit interacts with and inhibits the activity of PG. RGI and RGII are absent from the ML region, and exo-galactanase/β-galactosidase (β-Gase) and α-L-arabinofuranosidase (α-AFase) cleave the galactosyl and arabinayl residues, respectively, on the side chain of RGI. The ML dissolves due to degradation of HG pectin during fruit softening and the transition from mature green (MG) to red ripe (RR) tomato which causes the loosening of cell adhesion and leads to cell separation.