Dutch elm disease (DED), caused by (), is a destructive disease of American elm ( L.). The molecular mechanisms of resistance and susceptibility against DED in American elm are still largely uncharacterized. In the present study, we performed a transcriptome (RNA-sequencing; RNA-Seq) assembly of and compared the gene expression in a resistant genotype, 'Valley Forge', and a susceptible (S) elm genotype at 0 and 96 h post-inoculation of . A total of 85,863 non-redundant unigenes were identified. Compared to the previously characterized transcriptome, has 35,290 similar and 55,499 unique genes. The transcriptomic variations between 'Valley Forge' and 'S' were found primarily in the photosynthesis and primary metabolism, which were highly upregulated in the susceptible genotype irrespective of the inoculation. The resistance to DED was associated with the activation of RPM1-mediated effector-triggered immunity that was demonstrated by the upregulation of genes involved in the phenylpropanoids biosynthesis and PR genes. The most significantly enriched gene ontology (GO) terms in response to were response to stimulus (GO:0006950), response to stress (GO:0050896), and secondary metabolic process (GO:0008152) in both genotypes. However, only in the resistant genotype, the defense response (GO:0006952) was among the topmost significantly enriched GO terms. Our findings revealed the molecular regulations of DED resistance and susceptibility and provide a platform for marker-assisted breeding of resistant American elm genotypes.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8874831 | PMC |
http://dx.doi.org/10.3390/jof8020120 | DOI Listing |
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