ABSTRACT
Fusarium head blight (FHB) is a serious fungal disease affecting wheat and other cereals worldwide. This fungus causes severe yield and quality losses from a reduction in grain quality and contamination of grain with mycotoxins. Intensive breeding efforts led to the release of AAC Tenacious, which was the first spring wheat cultivar registered in Canada with a resistant (R) rating to FHB. To elucidate the physiological mechanisms of resistance, we performed histological and transcriptomic analyses of AAC Tenacious and a susceptible control Roblin after inoculation with Fusarium graminearum (Fg). The spikelet and rachis of infected wheat spikes were hand sectioned and monitored by confocal and fluorescent microscopy. Visible hyphae were observed within the inoculated spikelets for AAC Tenacious; however, the infection was largely restricted to the point of inoculation (POI), whereas the adjacent florets in Roblin were heavily infected. Significant cell wall thickening within the rachis node below the POI was evident in AAC Tenacious compared to Roblin in response to Fg inoculation. Rachis node and rachilla tissues from the POI and the rachis node below the POI were collected at 5 days post inoculation for RNAseq. Significant changes in gene expression were detected in both cultivars in response to infection. The rachis node below the POI in AAC Tenacious had fewer differentially expressed genes (DEGs) when compared to the uninoculated control, likely due to its increased disease resistance. Analysis of DEGs in Roblin and AAC Tenacious revealed the activation of genes and pathways in response to infection, including those putatively involved in cell wall modification and defense response.
ABSTRACT
The effects of Phytophthora infestans glucans, eicosapentaenoic acid (EPA) and isolates of this pathogen, on the differential expression of eight genes from the phenylpropanoid and the mevalonate (Ac-MVA) pathways were analyzed in potato by semi-quantitative RT-PCR and qRT-PCR. The application of EPA had an elicitor effect in Russet Burbank (RB) and Defender (DF) in response to inoculation with a US8 isolate of P. infestans, thereby reducing symptoms of late blight. Such effect was associated with the expression of PAL-1 and PAL-2, since the latter occurred only when EPA was followed by inoculation, whereas these genes were down-regulated in individual treatments RB + EPA, RB + US8, DF + EPA, and DF + US8. The glucan fraction did not by itself suppress phenylpropanoid genes, but its combination with the pathogen resulted in a down-regulation of PAL-1, PAL-2 and CHS. The addition of the glucan fraction to the elicitor EPA, had a negative effect (RB + EPA + GL + US8) since plants showed higher disease symptoms than the ones pretreated with water then infected with US8, and in comparison with RB + EPA + US8 and RB + GL + US8. Exclusive up-regulation of 4CL in DF + US11 and of CHS in DF + EPA + GL + US8, DF + EPA + US11, DF + GL + US11 and DF + EPA + GL + US11, where late blight lesions were not detected, could be associated with potato protection against late blight. Along with previous findings in this pathosystem, these data suggest that genetic resistance in potato against P. infestans is not the result of isolated reactions against the pathogen, but rather the combination of many factors in-line with a polygenic/horizontal resistance.
