by R.B. Pearce

The major hypotheses that have been proposed to explain the patterns of decay development and its restriction in the wood (xylem) of living trees are outlined briefly. The current understanding of the biochemical and physiological events that contribute to the protection of pre-existing functional sapwood is reviewed, with particular reference to the formation of reaction zones at the host-pathogen interface in Acer species, especially the European sycamore maple (Acer pseudoplatanus) in which the interactions between wood-inhabiting fungi and sapwood have been extensively investigated.Studies using conventional anatomical and biochemical approaches have been integrated with the application of advanced physical techniques (nuclear magnetic resonance [NMR] imaging, proton induced X-ray emission [PIXE] microanalysis and mapping, and electron paramagnetic resonance [EPR] spectroscopy), allowing a model describing the development and function of reaction zones in this species to be proposed.


Results from other woody angiosperms indicate that in some (e.g., European beech [Fagus sylvatica]) reaction zones may be essentially similar but that in others there may be significant differences. The implications of our developing understanding of antimicrobial defense in trees on the practice of arboriculture is discussed briefly.
Key Words. Antimicrobial defense; decay; compartmentalization; reaction zones; Acer pseudoplatanus; Fagus sylvatica.

Four principal models have been proposed to describe the development and restriction of decay in living trees. Until the 1970s, the heartrot concept was widely accepted (Boyce 1961; Peace 1962); decay was regarded as an essentially saprotrophic process, fungi entering through wounds or dead organs that exposed the nonliving heartwood, which was subsequently invaded, with little or no attack on the functional, living, sapwood. This was recognized as insufficient to account for the patterns of colonization observed behind many wounds and the occurrence of morphological and chemical changes at the margin between decay lesions and living sapwood (xylem), which have been interpreted as protective barriers that restrict the spread of infection. Boundaries formed at the interface between infected xylem and pre-existing sapwood were interpreted as dynamic defenses, retreating ahead of the advancing infection front, and have been termed reaction zones (Shain 1967, 1971, 1979), column boundary layers (Shortle and Smith 1990) or CBL reaction zones (Pearce 1996). Subsequent studies in a number of broad-leaved trees have refined this model, indicating that reaction zones form essentially static lesion boundaries that can retain their function for an extended time.


When these lesions expand, a volume of wood may become colonized with little or no expression of host responses, before a new reaction zone boundary is established (Pearce 1987, 1991; Boddy 1992). On the basis of patterns of discoloration and decay observed behind wounds, the compartmentalization of decay in trees (CODIT) model was proposed (Shigo and Marx 1977; Shigo 1979, 1984). According to this model, lesions in functional sapwood are bounded by 4 walls laid down in the wood, envisaged as essentially static barriers preventing the spread of infection. Walls 1 to 3, formed in wood present at the time of wounding are equivalent to reaction zones, but wall 4 is distinct, comprising a tissue laid down de novo by the cambium in the vicinity of wounds, and is the most durable of the compartmentalization walls.


Source : Journal of Arboriculture 26(1): January 2000

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