Vitenskapelig artikkel

Xylem defense wood of Norway spruce compromised by the pathogenic white-rot fungus Heterobasidion parviporum shows a prolonged period of selective decay

Nagy, Nina Elisabeth; Ballance, Simon; Kvaalen, Harald; Fossdal, Carl Gunnar; Solheim, Halvor; Hietala, Ari


Tidsskrift: Planta, vol. 236, p. 1125–1133, 2012

Utgiver: Springer

Utgave: 4

Internasjonale standardnumre:
Trykt: 0032-0935
Elektronisk: 1432-2048

Open Access: none


Heterobasidion parviporum, a common pathogenic
white-rot fungus in managed Norway spruce forests
in northern and central Europe, causes extensive decay columns
within stem heartwood of the host tree. Infected trees
combat the lateral spread of decay by bordering the heartwood
with a fungistatic reaction zone characterized by elevated
pH and phenol content. To examine the mode of
fungal feeding in the reaction zone of mature Norway
spruce trees naturally infected by H. parviporum, we conducted
spatial proWling of pectin and hemicellulose composition,
and established transcript levels of candidate fungal
genes encoding enzymes involved in degradation of the
diVerent cell wall components of wood. Colonized inner
heartwood showed pectin and hemicellulose concentrations
similar to those of healthy heartwood, whereas the carbohydrate
proWles of compromised reaction zone, irrespective of
the age of fungal activity in the tissue, indicated selective
fungal utilization of galacturonic acid, arabinose, xylose
and mannose. These data show that the rate of wood decay
in the reaction zone is slow. While the up-regulation of
genes encoding pectinases and hemicellulases preceded
that of the endoglucanase gene during an early phase of
fungal interaction with xylem defense, the manganese
peroxidase gene showed similar transcript levels during
diVerent phases of wood colonization. It seems plausible
that the reaction zone components of Norway spruce
interfere with both lignin degradation and the associated
co-hydrolysis of hemicelluloses and pectin, resulting in a
prolonged phase of selective decay.