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Genotype-by-genotype interactions reveal transcription patterns underlying resistance responses in Norway spruce to Heterobasidion annosum s.s

Summary

This study examined how different types of Norway spruce trees respond to infection by a fungus that causes root rot. Researchers found that the spruce tree’s genetics are more important than the fungus’s virulence in determining disease severity. Resistant tree clones activate specific defense genes early in infection, particularly genes related to pathogen recognition, while susceptible trees mount a delayed and broader response. Understanding these genetic differences could help with breeding more resistant trees for forests.

Background

Norway spruce is economically important in European forests but susceptible to root rot caused by Heterobasidion annosum. Disease resistance in conifers involves quantitative disease resistance (QDR) with complex genetic components. Understanding how host and pathogen genotypes interact at the molecular level can illuminate resistance mechanisms.

Objective

To investigate how variation in virulence in H. annosum s.s. induces different transcriptional responses in Norway spruce genotypes with varying resistance levels. To test whether host genotypes respond differently to different pathogen isolates and whether these differences are accompanied by distinct transcriptional reprogramming.

Results

Host genotype was the strongest predictor of disease phenotype, especially early in infection. Resistant clones showed distinct upregulated genes at 5 dpi, particularly leucine-rich repeat (LRR) family genes, while susceptible clone 1977 showed extensive transcriptional changes at 21 dpi. Different host genotypes employed distinct defense modules and genes, suggesting multiple pathways can achieve similar resistance phenotypes.

Conclusion

Phenotypic resistance to H. annosum in Norway spruce can be governed by different defense modules and genes depending on host genotype. Recognition of the pathogen through LRR genes appears crucial for limiting pathogen spread. Disease outcome is determined early in the interaction, with host genotype having stronger effects than pathogen virulence.
  • Published in:BMC Plant Biology,
  • Study Type:Experimental Study,
  • Source: PMID: 41053581
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