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

Summary

Researchers studied how different spruce trees resist a wood-rotting fungus by examining which genes turn on and off during infection. They found that resistant trees quickly recognize the fungus and strengthen their cell walls, while susceptible trees have delayed responses. Interestingly, different resistant trees sometimes use different defense strategies to achieve similar protection, suggesting multiple genetic pathways can lead to the same outcome.

Background

Quantitative disease resistance (QDR) in plant-pathogen interactions involves complex genetic and molecular networks that are not well understood. The Norway spruce-Heterobasidion annosum pathosystem is an economically important forest disease, with resistance involving multiple genetic loci with small to moderate effects. Understanding how different host and pathogen genotypes interact at the molecular level could improve resistance breeding strategies.

Objective

To investigate how variation in virulence of H. annosum s.s. isolates induces different transcriptional responses in Norway spruce genotypes with varying resistance levels. The study tested three hypotheses: (i) host and pathogen genotypes affect disease symptoms, (ii) host genotypes respond differently depending on the isolate, and (iii) this is accompanied by distinct transcriptional reprogramming.

Results

Host genotype was the strongest predictor of disease phenotype, particularly early in infection. Interactions resulting in longer necrotic lesions were associated with larger numbers of differentially expressed genes. Each host-pathogen interaction displayed distinct transcriptional responses with different defense modules activated. Leucine rich repeat (LRR) family genes were upregulated in resistant clones and downregulated in susceptible clones, suggesting pathogen recognition is key to limiting fungal spread.

Conclusion

Phenotypic resistance responses in Norway spruce to H. annosum s.s. can be governed by different defense modules and genes depending on the specific host-pathogen interaction. Early activation of key defense mechanisms, including recognition genes (LRRs) and cell wall reinforcement genes, appears critical for successful resistance. These findings suggest that similar disease outcomes can result from different molecular mechanisms depending on the genotypic combination.
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