Table 1. Summary of membrane, cytosol, and cell wall responses to wounding (modified by Biggs after Bostock and Stermer 1989).  Table begins with injury or wound stimulus at the top and proceeds to cell division, wound periderm formation, and vascular occlusion at the bottom.

INJURY OR WOUND STIMULUS

 

IMMEDIATE OR RAPID RESPONSES

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

SLOW RESPONSES

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 MEMBRANES

 

Depolarization of cell membranes

 

Net K+ Cl- efflux

 

Net H+ Ca2+ influx

 

Loss of compartmentation and release of lipid-degrading and oxidative enzymes

 

Deacylation of membrane lipids

 

Generation of local and systemic wound signals (action potentials, traumatin, Ricca's factor (?))

 

Stimulation of callose synthetase, cellulose synthetase, and ACC synthetase

 

Repolarization of membrane potential

 

 

Restoration of membrane structure

 

Restoration of ion transport mechanisms

 CYTOSOL

 

Cytoplasmic aggregation

 

Generation of volatiles (aldehydes, ethane, ethylene, and other products of lipid peroxidation)

 

Wound respiration

 

Reactive oxygen species

 

ABA synthesis

 

Ethylene from ACC

 

Generation of other second messengers (phosphoinositides, Ca/calmodulin)

 

Enhanced transcriptional and translational activities

 

Activation of TCA cycle

 

Elevated cyanide-insensitive respiration

 

Accelerated catabolism of sugars by glycolytic and pentose pathways

 

Biosynthesis of phenylpropanoids, isoprenoids, and polyketides

 

Induction of proteinase inhibitors, chitinase, glucanase, acidic peroxidases, phenoloxidases, and enzymes for suberin synthesis

 

 CELL WALL

 

 

 

 

 

 

 

 

 

 

 

Stimulation of polysaccharidases (?), and basic peroxidases

 

 

 

Release of oligogalacturonides (?)

 

 

 

 

 

 

 

 

 

 

 

 

 

Papillae and callose deposition

 

Ca2+ and Si deposition

 

Modification by phenolic esters, lignin, HRGPs

 

 

 

 

 

 

Suberin deposition

CELL DIVISION, WOUND PERIDERM FORMATION AND VASCULAR OCCLUSION

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