Such strategists have their spores colonise the (now dysfunctional) sapwood after a wound exposes what would otherwise have been functional sapwood. Such strategists are adapted to a wood environment with high oxygen content and (initially) high moisture levels (Boddy, 2001; Rayner, 1993; Rayner & Boddy, 1988; Schwarze et al., 2000). Cankers may also facilitate the establishment for spores of such strategists, in particular instances (Shigo, 1986).
Sapwood-exposed strategists are typically rapid in colonisation rate, though do not begin to cause decay until the wood dries out (Schwarze et al, 2000); by this point, non-decay-causing organisms have likely already begun to colonise, and may in fact aid with fungal succession and wood degradation (Rayner, 1993; Schwarze et al., 2000; Shigo, 1991). As such, there is a (brief) ‘latent’ period in between infection and decay. During this delay, the fungus will take advantage of readily-available food sources such as sugars, using the energy to fuel its rapid colonisation habit. Such rapid establishment means the tree does not have enough time to properly compartmentalise the attack around the wounded area (Rayner & Boddy, 1988; Schwarze et al., 2000). Some of these strategists also deploy offensive mechanisms to further damage the tree, such as via the secretion of toxins to kill or damage parenchyma cells.
The decay column that manifests following fungal establishment is largely axial in spread, progressing vertically from the wound site with – at least initially – little radial spread. The decayed area will be surrounded by a discoloured margin, where the tree has deposited tyloses, suberin, and phenols, in an attempt to compartmentalise the decay process by shutting down and clogging its vascular tissues (Boddy, 2001; Dujesiefken & Liese, 2015; Shigo, 1991; Weber & Mattheck, 2003). Discolouration and decay extent both vary depending upon the species of fungus and the tree species’ characteristics (intrinsic), as well as the environment in which the host tree resides (extrinsic) (Rayner, 1993; Rayner & Boddy, 1988).
In certain instances, numerous unspecialised strategists may colonise a tree in different regions, surrounding either the same wound or, if the tree has many wounds, various ones (Boddy, 2000). This can lead to intricate patterns of decay and barrier zones between each different hyphal network, at times with barriers being visibly breached on numerous occasions. Ultimately, it is critical that invading pathogens create and retain their own zones within the wood structure, protecting the hyphal network from both tree defence mechanisms, mycoparasites, and other invading pathogens (Boddy & Rayner, 1983; Shain, 1979; Shigo, 1986).
Furthermore, such strategists possess a wide range of ‘sub-colonisation’ strategies, varying from the ruderal (saprophytic) mold fungi (Hyphomycetes) to the combative (parasitic) Basidiomycetes (Schwarze et al., 2000). Ruderal strategists do not typically degrade wood but merely discolour it, though may initiate decay that may, as already suggested, initiate succession by higher-tier Basidiomycetes of the same site. This is because ruderal strategists tend to enter early, colonise, and exit, before conditions become undesirable (due to lowering nutrient availability, competition from other decay organisms, desiccation of substrate, etc). They are largely non-selective with regards to species preference (Boddy, 2001).
As a partial aside, unspecialised opportunists will also attack incredibly young seedlings. Seedlings, until a certain age (species-specific, in part, though also driven by environmental conditions – may be from 5 days to 2+ weeks), lack the ‘mature’ tissue and resistance to pathogens that established ones have (this occurs when pectin begins to convert to calcium pectate within cell walls). This means seedlings are susceptible to unspecialised opportunists, particularly those within the soil. Depending upon the extent of soil-based inoculum, seedlings may in fact be killed before they even emerge from the soil (high inoculum potential). If the inoculum base is lower, seedlings may instead be killed post-emergence. In such instances, where localised humidity is high due to an abundance of seedlings creating a humid micro-climate and high rainfall (or artificial watering), fungal mycelium may spread across the surface from hypocotyl to hypocotyl – such rapid spread is aided by better aeration when compared to soil aeration (Garrett, 1970). Such a concept is termed ‘damping-off’ disease.
Boddy, L. (2000) Interspecific combative interactions between wood-decaying basidiomycetes. FEMS Microbiology Ecology. 31 (3). p185-194.
Boddy, L. & Rayner, A.. (1983) Origins of decay in living deciduous trees: the role of moisture content and a re-appraisal of the expanded concept of tree decay. New Phytologist. 94 (4). p623-641.
Dujesiefken, D. & Liese, W. (2015) The CODIT Principle: Implications for Best Practices. USA: International Society of Arboriculture.
Garrett, S. (1970) Pathogenic Root-Infecting Fungi. USA: Cambridge University Press.
Mattheck C., Bethge, K., & Weber, K. (2015) The Body Language of Trees: Encyclopedia of Visual Tree Assessment. Germany: Karlsruhe Institute of Technology.
Rayner, A. (1993) New avenues for understanding processes of tree decay. Arboricultural Journal. 17 (2). p171-189.
Rayner, A. & Boddy, L. (1988) Fungal Decomposition of Wood: It’s Ecology and Biology. UK: John Wiley & Sons.
Schwarze, F., Engels, J., & Mattheck, C. (2000) Fungal Strategies of Wood Decay in Trees. UK: Springer.
Shain, L. (1979) Dynamic responses of differentiated sapwood to injury and infection. Phytopathology. 69 (10). p1143-1147.
Shigo, A. (1986) A New Tree Biology. USA: Shigo and Trees Associates.
Shigo, A. (1991) Modern Arboriculture. USA: Shigo and Trees Associates.
Weber, K. & Mattheck, C. (2003) Manual of Wood Decays in Trees. UK: The Arboricultural Association.
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