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Sammanfattning

Heterobasidion parviporum Niemela & Korhonen is responsible for the majority of decay in conifers in northern Europe, which causes severe economic losses. In nature, heterokaryotic isolates of H. parviporum cause infection in Norway spruce (Picea abies (L.) Karst.). However, little is known on whether homokaryons of H. parviporum can infect trees under field conditions. In this study, 40-year-old clonal Norway spruce stems and roots were inoculated with a homokaryotic isolate of H. parviporum under field conditions. After four months, the infection frequency and necrotic lesion lengths were recorded. The homokaryon caused infection and provoked the development of necrotic lesions. Necrotic lesions were larger in roots than in stems. Among the studied Norway spruce genotypes, a Russian clone had the smallest necrotic lesions, whereas a Finnish clone developed the largest necrotic lesions. Clones with higher growth rates were more sensitive to fungal infection and wound damage. Under microscopic observation, H. parviporum grew adpressed to lumen cell walls, colonized tracheids next to rays, and induced lignification in cell walls close to the point of inoculation. This study provides a starting point for further studies on the ability of homokaryons to cause infection under field conditions and for discussions on factors affecting the resistance of Norway spruce against H. parviporum.

Nyckelord

Heterobasidion parviporum; Picea abies; homokaryon; susceptibility; clonal material

Publicerad i

Canadian Journal of Forest Research
2015, volym: 45, nummer: 3, sidor: 227-235
Utgivare: CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS

SLU författare

  • Keriö, Susanna

    • Helsingin yliopisto

  • Daniel, Geoffrey

    • Institutionen för skogens produkter, Sveriges lantbruksuniversitet

Associerade SLU-program

SLU Nätverk växtskydd

UKÄ forskningsämne

Skogsvetenskap

Publikationens identifierare

  • DOI: https://doi.org/10.1139/cjfr-2014-0247

Permanent länk till denna sida (URI)

https://res.slu.se/id/publ/76080