Su Zhiyi, Lu Wanhong, Lin Yan, Luo Jianzhong, Liu Guo, Huang Anying
Institute of Fast-Growing Trees, Chinese Academy of Forestry, Zhanjiang 524022, China.
College of Forestry and Grassland, Nanjing Forestry University, Nanjing 210037, China.
Curr Issues Mol Biol. 2024 Sep 27;46(10):10854-10879. doi: 10.3390/cimb46100645.
Selecting high-quality varieties with disease resistance by artificial crossbreeding is the most fundamental way to address the damage caused by spp. in eucalypt plantations. However, understanding the mechanism of disease-resistant heterosis occurrence in eucalypts is crucial for successful crossbreeding. Two eucalypt hybrids, the susceptible EC333 (H1522 × unknown) and the resistant EC338 (W1767 × P9060), were screened through infection with isolates, a pathogen that causes eucalypt leaf blight. RNA-Seq was performed on the susceptible hybrid, the disease-resistant hybrid, and their parents. The gene differential expression analysis showed that there were 3912 differentially expressed genes between EC333 and EC338, with 1631 up-regulated and 2281 down-regulated genes. The expression trends of the differential gene sets in P9060 and EC338 were similar. However, the expression trend of W1767 was opposite that of EC338. The similarity of the expression and the advantage of stress resistance in suggested that genes with significant differences in expression likely relate to disease resistance. A GSEA based on GO annotations revealed that the carbohydrate binding pathway genes were differentially expressed between EC338 and EC333. The gene pathways that were differentially expressed between EC338 and EC333 revealed by the GSEA based on KEGG annotations were the sesquiterpenoid and triterpenoid biosynthesis pathways. The alternative splicing analysis demonstrated that an AS event between EC338 and EC333 occurred in LOC104426602. According to our SNP analysis, EC338 had 626 more high-impact mutation loci than the male parent P9060 and 396 more than the female parent W1767; W1767 had 259 more mutation loci in the downstream region than EC338, while P9060 had 3107 fewer mutation loci in the downstream region than EC338. Additionally, EC338 had 9631 more mutation loci in the exon region than EC333. Modules were found via WGCNA that were strongly and oppositely correlated with EC338 and EC333, such as module MEsaddlebrown, likely associated with leaf blight resistance. The present study provides a detailed explanation of the genetic basis of eucalypt leaf blight resistance, providing the foundation for exploring genes related to this phenomenon.
通过人工杂交选育具有抗病性的优质品种是应对桉树林中 spp. 造成损害的最根本途径。然而，了解桉树抗病杂种优势发生的机制对于成功杂交育种至关重要。通过用引起桉树叶枯病的病原体 分离株感染，筛选出两个桉树杂交种，易感的 EC333（H1522×未知）和抗病的 EC338（W1767×P9060）。对易感杂交种、抗病杂交种及其亲本进行了 RNA-Seq 分析。基因差异表达分析表明，EC333 和 EC338 之间有 3912 个差异表达基因，其中 1631 个基因上调，2281 个基因下调。差异基因集在 P9060 和 EC338 中的表达趋势相似。然而，W1767 的表达趋势与 EC338 相反。表达的相似性和 中的抗逆优势表明，表达有显著差异的基因可能与抗病性有关。基于 GO 注释的 GSEA 分析表明，碳水化合物结合途径基因在 EC338 和 EC333 之间差异表达。基于 KEGG 注释的 GSEA 分析揭示的 EC338 和 EC333 之间差异表达的基因途径是倍半萜和三萜生物合成途径。可变剪接分析表明，EC338 和 EC333 之间在 LOC1044266 和 EC333 之间发生了 AS 事件。根据我们的 SNP 分析，EC338 比父本 P9060 多 626 个高影响突变位点，比母本 W1767 多 396 个；W1767 在下游区域比 EC338 多 259 个突变位点，而 P9060 在下游区域比 EC338 少 3107 个突变位点。此外，EC338 在外显子区域比 EC333 多 9631 个突变位点。通过 WGCNA 发现了与 EC338 和 EC333 强烈且相反相关的模块，如模块 MEsaddlebrown，可能与叶枯病抗性有关。本研究详细解释了桉树叶枯病抗性的遗传基础，为探索与此现象相关的基因提供了基础。
