1CRC for Sustainable Production Forestry, GPO Box 252-12, Hobart, TAS 7001, AU; 2Dept. Agricultural Science, Univ. Tasmania, GPO Box 252-54, Hobart, TAS 7001, AU; 3CSIRO, Forestry and Forestry Products, GPO Box 252-12, Hobart, TAS 7001, AU; 4School of Biological Sciences, Univ. Birmingham, B15 2TT, UK

Background and Objectives
In Tasmania plantations E. nitens retains dead branches, which results in serious problems with wood quality. Consequently green pruning at a young age is essential for producing high quality logs and veneer from plantations over a short rotation of 20-25 years. In a preliminary survey, the authors have found an unacceptably high incidence of decay columns originating from larger diameter pruned stubs in 8 year E. nitens pruned in two lifts at 3 and 5 years. Current research is systematically quantifying the incidence of decay associated with pruning wounds in plantation E. nitens under defined site conditions, pruning seasons and methods. Commercially pruned E. nitens plantations have only been established within the last decade and it is not known if decay introduced into the knotty core of the pruned stem will have spread to the clearwood at harvest. Therefore, one of the key questions to be answered for the forest industry today is: 'How effective is antimicrobial defence in E. nitens?' Although a recent review has outlined mechanisms which restrict the development of decay in living trees [1], it is based primarily on studies with northern hemisphere species, and there have been no equivalent studies of antimicrobial defence in eucalypt wood.

Results and Conclusions
In practice, not all branches are living (green) when pruned. Variations in growth at different sites dictate the proportions of green, senescent and dead branches at first lift pruning. The incidence of decay columns is most strongly correlated with the number of large diameter green pruned branches. In comparison, the extension of naturally-occurring decay lesions associated with unpruned branches appears contained, restricted by a purple reaction zone with a high tannin component produced in challenged sapwood and characterised by tylosed vessels. Formation of a suberized circumferential barrier zone comprised of undifferentiated parenchyma is also frequently observed. Distinct kino veins are not normally formed by E. nitens. Fungi have not been successfully isolated from the reaction zones and associated clearwood and chromatographic comparisons of extracts from clearwood, reaction zones and decayed tissue have revealed chemical changes, including the accumulation of potentially important antifungal compounds, in the reaction zone. The transverse protective zone formed across the branch collar region of senescing branches appears similar to these lesion margin reaction zones.

Gravimetric determinations show the xylem water content of E. nitens to be particularly high (174% dry wt). The purple reaction zone is often drier than adjacent sapwood. Proton induced X-ray emission microanalysts and mapping showed no major disparity in the distribution of mineral elements at lesion margins, and electron spin resonance spectroscopy indicated that long-lived free radicals were absent from the reaction zones.in these respects the defence strategy of E. nitens appears different from that described from the sapwood of some other angiosperms [1]. Moisture content patterns across the reaction zone and adjacent sapwood were more similar to those reported in conifers than other angiosperms. Water saturation (and consequent anoxia) that appears normal in this species may confer a high level of intrinsic protection on sapwood as long as it remains functional and its physical integrity remains uncompromised by wounding. Osmotically driven water accumulation and the formation of a free radical-rich protective polymer in defence, as reported in Acer pseudoplatanus [1, 2] does not appear important in this eucalypt. Whether the apparent absence of these components of the xylem defence response increases long-term vulnerability of E. nitens to decay damage, or whether other mechanisms operate successfully, remains to be determined.

1. Pearce RB, 1996. New Phytologist 132, 203-233.
2. Pearce RB, Edwards PP, Green TL, Anderson PA, Fisher BJ, Carpenter TA, Hall LD, 1997. Physiological and Molecular Plant Pathology 50, 371-390.