Islam Md Tabibul, Coutin Jose Freixas, Shukla Mukund, Dhaliwal Amandeep Kaur, Nigg Martha, Bernier Louis, Sherif Sherif M, Saxena Praveen K
Alson H. Smith Jr. Agricultural Research and Extension Center, School of Plant and Environmental Sciences, Virginia Tech, Winchester, VA 22602, USA.
Department of Plant Agriculture, Gosling Research Institute for Plant Preservation (GRIPP), University of Guelph, Guelph, ON N1G 2W1, Canada.
J Fungi (Basel). 2022 Jan 26;8(2):120. doi: 10.3390/jof8020120.
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.
荷兰榆树病（DED）由（）引起，是美国榆树（榆属）的一种毁灭性病害。美国榆树对DED的抗性和易感性分子机制在很大程度上仍未明确。在本研究中，我们对（）进行了转录组（RNA测序；RNA-Seq）组装，并比较了抗性基因型‘Valley Forge’和易感（S）榆树基因型在接种（）后0小时和96小时的基因表达。共鉴定出85,863个非冗余单基因。与先前表征的（）转录组相比，（）有35,290个相似基因和55,499个独特基因。发现‘Valley Forge’和‘S’之间的转录组差异主要存在于光合作用和初级代谢中，无论是否接种（），易感基因型中的这些过程均高度上调。对DED的抗性与RPM1介导的效应子触发免疫的激活有关，这通过参与苯丙烷类生物合成的基因和病程相关（PR）基因的上调得以证明。两种基因型中响应（）最显著富集的基因本体（GO）术语是对刺激的响应（GO:0006950）、对胁迫的响应（GO:0050896）和次生代谢过程（GO:0008152）。然而，仅在抗性基因型中，防御反应（GO:0006952）是最显著富集的GO术语之一。我们的研究结果揭示了DED抗性和易感性的分子调控机制，并为抗性美国榆树基因型的标记辅助育种提供了一个平台。
