Fungal colonisation strategies Pt. I: Heart rot

There exist four different colonisation strategies of a living tree by wood-decay fungi: heart rot (heartwood-exposed), unspecialised opportunism (sapwood-exposed), specialised opportunism (sapwood-intact), and active pathogenesis (Boddy, 2001; Rayner, 1993; Rayner & Boddy, 1988; Schwarze et al., 2000). Over the coming week or so, I’ll be looking at each strategy. We shall begin with heart rot.

Heart rot

In simple terms, this strategy involves colonisation of heartwood – via an entry point where heartwood becomes exposed – and subsequent decay of such heartwood (or core) of the host, where parenchyma (living) cells are lacking and conditions are very gaseous (Boddy, 2001; Rayner & Boddy, 1988; Schwarze, 2008). Colonisation is considered to be through heartwood-exposed wound surfaces, or alternatively via exposed heartwood from dead or diseased areas of the tree that are old enough to contain heartwood. Entry via such mechanisms can be divided into two distinct segments: top-rot (colonisation originates at the crown and progresses downwards) and butt-rot (colonisation originates at the root collar-butt interface and works upwards). For butt-rots, colonisation can further be divided, with entry being via root-mycelium contact, or by fungal spores (Rayner & Boddy, 1988). Rarely do butt rots cause hollows more than a few feet up into the trunk (Shigo, 1986).

Such strategists are particularly stress-tolerant, predominantly because conditions for decay are initially very unsuitable deep within the heartwood of the host. The lack of oxygen, high levels of carbon dioxide, undesirable moisture levels (particularly if bacterial wetwood is present – this will occur if bacteria are the pioneer invaders of a site, and not fungal pathogens), and abundance of inhibiting compounds (tannins), mean decay will be a very slow process and may take many years to even initiate substantially. Species that adopt this strategy therefore are largely non-combative, very slow with regards to their decay and colonisation of the heartwood, and may well be species-specific; or at least show certain levels of host species-preference (Boddy, 2001; Boddy & Rayner, 1983; Cartwright & Findlay, 1958; Rayner & Boddy, 1988; Shigo, 1986; Weber & Mattheck, 2003). The predominant reason behind such frequently-observed selectivity is suspected to be due to the fact that different species of host possess vastly different characteristics with regards to heartwood formation and properties, and by limiting host preference the fungal species directly reduce their potential fungal competitor range to, in some instance, almost zero (Rayner & Boddy, 1988). Species-specificness ultimately varies between heart rot strategists, therefore; a continuum, of sorts (Rayner & Boddy, 1988). Genus-specific strategists include Fistulina hepatica (Quercus spp.), Phellinus pomaceus (Prunus spp.), and Porodaedalea pini (Pinus spp.), whilst generalist strategists include Armillaria spp. and Heterobasidion annosum. Rayner and Boddy (1988) also note that Laetiporus sulphureus may colonise seemingly unrelated species such as Castanea spp., Quercus spp., Salix spp., and Taxus spp.

This oddly-shaped Fistulina hepatica, a heart rot strategist, was found (by me) at the base of a very mature Quercus robur.

In spite of their largely non-combative ability, both with regards to colonisation of wood and competition against other fungi, their intricate specialisms that have optimised them for heartwood decay enable them to create large individual territories amongst the expansive heartwood extent within their host. Mycoparasites (fungal parasites that predate upon other fungi) may however be a potentially limiting factor, in certain instances, where such fungal parasites establish within the decaying wood zone(s) and attack the wood-decaying fungi present – as may fungal viruses (Badalyan et al., 2004; Boddy, 2000; Boddy & Rayner, 1983; Shigo, 1986).

Research by Highley et al. (1983) also suggests that the lack of difference in performance under low oxygen and high carbon dioxide regime levels for heart rot strategists means they may have evolved to become so specialised by adapting to species-specific heartwood traits (pH, volatiles, extractives, etc) – such as with Laetiporus sulphureus and its ability to tolerate tannin-rich and acetic acid-rich wood, which correlates with the low pH of Quercus spp. heartwood, and its high tannin levels (Hintikka 1969, Hintikka 1971, Rayner & Boddy, 1988).

In this image (taken by me) a mature Pinus nigra, with major storm damage upon its stem, has been colonised by the heart rot strategist Porodaedalea pini.

Heart rot is typically non-fatal for trees (at least, in the direct sense – the tree may die as a result failure induced by the decay), in the sense that it is considered to be more economically destructive to foresters than it is the health and longevity of the tree (Rayner, 1993, Rayner & Boddy, 1988). Because such strategists largely lack the ability to invade intact sapwood, their extent is confined to the heartwood of the host, thereby enabling the tree to continue in its metabolic pursuits without marked hindrance. However, death can be caused when heartrot strategists that are able to attack sapwood (through suspected active pathogenesis – Phellinus pomaceus), for the purpose of creating fruiting bodies (on sites where exposed heartwood does not exist) and for means of continued colonisation (Mattheck et al., 2015; Rayner & Boddy, 1988), do so extensively – to the point that the stem may be girdled, or the sapwood significantly damaged. Such a means of sapwood attack is through the development of a canker, initiated by the creation of a thick mycelial pad, which serves to force bark outwards and thus enable for an exit point (Rayner & Boddy, 1988).

References

Badalyan, S., Innocenti, G., & Garibyan, N. (2004) Interactions between xylotrophic mushrooms and mycoparasitic fungi in dual-culture experiments. Phytopathologia Mediterranea. 43 (1). p44-48.

Boddy, L. (2000) Interspecific combative interactions between wood-decaying basidiomycetes. FEMS Microbiology Ecology. 31 (3). p185-194.

Boddy, L. (2001) Fungal community ecology and wood decomposition processes in angiosperms: from standing tree to complete decay of coarse woody debris. Ecological Bulletins. 49 (1). p43-56.

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.

Cartwright, K. & Findlay, W. (1958) Decay of Timber and its Prevention. 2nd ed. London: HMSO.

Highley, T., Bar-Lev, S., Kirk, T., & Larsen, M. (1983) Influence of O2 and CO2 on wood decay by heartrot and saprot fungi. Phytopathology. 73 (4). p630-633.

Hintikka, V. (1969) Acetic acid tolerance in wood – the litter decomposing Hymenomycetes. Karstenia. 10 (1). p177-183.

Hintikka, V. (1971) Tolerance of some wood decomposing basidiomycetes to aromatic compounds related to lignin degradation. Karstenia. 12 (1). p46-52.

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.

Shigo, A. (1986) A New Tree Biology. USA: Shigo and Trees Associates.

Weber, K. & Mattheck, C. (2003) Manual of Wood Decays in Trees. UK: The Arboricultural Association.

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