The fungal plant pathogen Sphaerulina musiva (Ascomycota) causes Septoria stem canker, the most economically damaging disease of Populus plantations in North America, yet the genetic determinants of host resistance remain uncharacterized in hybrid poplar. Using an inoculation experiment with the 52-124 pseudo-backcross family of Populus trichocarpa × Populus deltoides (TD × D) hybrid poplar, a single significant QTL was identified on Chromosome 16 (LOD = 4.93) associated with both stem canker count and disease severity score. Transcriptomic analysis of two resistant and two susceptible genotypes across a 72-hour infection time course identified a single differentially expressed gene within the QTL candidate gene window: Podel.16G125900, a putative leucine-rich repeat receptor-like protein (LRR-RLP) with homology to receptor-like protein 33 in Arabidopsis thaliana. Podel.16G125900 is located 3001 bp (0.019 cM) upstream of the QTL peak and showed a strong infection-induced upregulation in susceptible genotype 852 (log2 fold-change = 20.47) and higher baseline expression in resistant genotypes relative to susceptible genotypes across all infection time points, consistent with a resistance mechanism in which expression level contributes to the degree of resistance conferred. Two P. trichocarpa homologs were not differentially expressed and differ substantially in sequence content, suggesting the resistance function is specific to the resistant P. deltoides lineage. These findings identify Podel.16G125900 as a strong candidate gene underlying quantitative resistance mechanisms modulating Septoria stem canker resistance in the 52-124 family of TD × D hybrid poplar and provide a target for future functional validation and marker-assisted resistance breeding.
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It is demonstrated that linker-free PROTACs can outperform traditional designs, marking a paradigm shift in PROTAC development for targeted protein degradation.
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