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Abstract

Aspects of the degradation of non-cellulosic polysaccharides (pectins, hemicelluloses) in spruce and ash sapwood by the brown rot fungus Postia placenta was investigated using transmission electron microscopy coupled with immunocytochemistry. Degradation of non-cellulosic polysaccharides and changes in ultrastructure were initiated in the compound middle lamella (CML)/middle lamella cell corner (MLcc) regions of xylem cells; sites that were remote from hyphal colonization in the cell lumen. Degradation of the S-3 layer was also detected in both wood species at early stages of decay. Apart from early stages of attack, the degradation patterns differed greatly between spruce and ash. Spruce showed three patterns of hemicellulose degradation in the secondary cell walls of tracheids, while ash showed a single pattern in fibers. Spruce parenchyma cells also showed lower resistance to decay than tracheids, whereas ash parenchyma. cells showed higher resistance than fibers. Together, degradation of xylem cells by P. placenta differs between spruce (softwood) and ash (hardwood) even though they show similar initial degradation in CML/MLcc regions and the S-3 layer. The overall degradation patterns observed, particularly in spruce differ from previous ideas and generally accepted decay patterns produced by brown rot fungi in wood. (C) 2015 Elsevier Ltd. All rights reserved.

Keywords

Brown rot decay; Middle lamella decay; Immunocytochemistry; Hemicellulose; Pectin; Postia placenta

Published in

International Biodeterioration and Biodegradation
2015, volume: 103, pages: 161-178

SLU Authors

  • Kim, Jongsik

    • Department of Forest Products, Swedish University of Agricultural Sciences

  • Gao, Jie

    • Department of Forest Products, Swedish University of Agricultural Sciences

  • Daniel, Geoffrey

    • Department of Forest Products, Swedish University of Agricultural Sciences

Associated SLU-program

SLU Plant Protection Network

UKÄ Subject classification

Wood Science
Forest Science

Publication identifier

  • DOI: https://doi.org/10.1016/j.ibiod.2015.05.005

Permanent link to this page (URI)

https://res.slu.se/id/publ/69742