ArticleBMC plant biology2025
Genotype-by-genotype interactions reveal transcription patterns underlying resistance responses in Norway spruce to Heterobasidion annosum s.s.
Article in BMC plant biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The expression of the genetic components involved in quantitative disease resistance (QDR) are often not well understood and analyses of genotype-by-genotype interactions can shed light on how the resistance and the activation of resistance strategies vary across interactions. To deepen the knowledge on QDR and the molecular interactions in the Norway spruce (Picea abies)- Heterobasidion annosum s.l.. pathosystem we inoculated ten relatively resistant spruce clones with four H. annosum s.s. isolates with varying virulence and determined the disease phenotypes. Thereafter we analysed the transcriptome in nine interactions between three spruce clones and three isolates. We tested the hypotheses that (i) differences among host and pathogen genotypes affect the disease symptoms; (ii) host genotypes respond differently depending on the isolate they were challenged with and (iii) this effect is accompanied by distinct transcriptional reprogramming. We found varying levels of disease expression among the interactions influenced by both host and pathogen genotypes. The host genotype was the strongest predictor of the disease phenotype, especially early in the interaction. The transcriptional responses differed between the three clones, interactions resulting in longer necrotic lesions were associated with larger numbers of differentially expressed genes. Despite this and the strong impact of the host genotype on disease phenotype each interaction displayed distinct transcriptional responses in a host genotype. These results indicate that phenotypic resistance responses can be governed by different defence modules and genes in Norway spruce. For instance, several leucine rich repeat family genes were found to be upregulated in the clones with higher resistance and downregulated in the clone with the lower resistance indicating that recognition of the pathogen may be one of the keys to limiting H. annosum s.s. spread in Norway spruce.
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