Zhengzhou Fruit Research Institute, Chinese Academy of Agricultural Sciences, Zhengzhou, China.
College of Horticulture and Forestry Sciences, Huazhong Agricultural University, Wuhan, China.
PLoS One. 2019 Feb 19;14(2):e0211913. doi: 10.1371/journal.pone.0211913. eCollection 2019.
Kiwifruit bacterial canker is a devastating disease threatening kiwifruit production. To clarify the defense mechanism in response to Pseudomonas syringae pv. actinidiae (Psa), we observed phenotypic changes in resistant Huate (HT) and susceptible Hongyang (HY) kiwifruit varieties at 0, 12, 24, 48, 96, and 144 hour after inoculation (hai) with Psa. Brown lesions appeared in the inoculation areas 12 hai in HY shoots, and the lesion length gradually increased from 24 to 144 h. In contrast, no lesions were found in HT shoots at any time points. Furthermore, RNA-seq analysis showed significantly more differentially expressed genes between HT and HY at 12 hai than at any other time point. According to weighted gene co-expression network analysis, five modules were notably differentially expressed between HT and HY; pathway mapping using the Kyoto Encyclopedia of Gene and Genomes database was performed for the five modules. In MEgreenyellow and MEyellow modules, pathways related to"plant-pathogen interaction", "Endocytosis", "Glycine, serine and threonine metabolism", and "Carbon fixation in photosynthetic organisms" were enriched, whereas in the MEblack module, pathways related to "protein processing in endoplasmic reticulum", "plant-pathogen interaction", and "Glycolysis / Gluconeogenesis" were enriched. In particular, the Pti1 and RPS2 encoding effector receptors, and the NPR1, TGA, and PR1 genes involved in the salicylic acid signaling pathway were significantly up-regulated in HT compared with HY. This indicates that the effector-triggered immunity response was stronger and that the salicylic acid signaling pathway played a pivotal role in the Psa defense response of HT. In addition, we identified other important genes, involved in phenylpropanoid biosynthesis and Ca2+ internal flow, which were highly expressed in HT. Taken together, these results provide important information to elucidate the defense mechanisms of kiwifruit during Psa infection.
猕猴桃溃疡病是一种毁灭性疾病，严重威胁猕猴桃的生产。为了阐明猕猴桃对丁香假单胞菌 pv.actinidiae (Psa)的防御机制，我们观察了接种 Psa 后抗性品种‘华特’（HT）和感病品种‘红阳’（HY）猕猴桃在 0、12、24、48、96 和 144 小时（hai）时的表型变化。HY 猕猴桃接种后 12 小时叶片接种部位出现褐色病斑，病斑长度从 24 小时逐渐增加到 144 小时。而 HT 猕猴桃在任何时间点都没有发现病斑。此外，RNA-seq 分析表明，HT 和 HY 在接种后 12 小时的差异表达基因明显多于其他任何时间点。根据加权基因共表达网络分析，HT 和 HY 在 12 hai 时的 5 个模块差异表达明显；使用京都基因与基因组百科全书数据库对这 5 个模块进行通路映射。在 MEgreenyellow 和 MEyellow 模块中，富集了与“植物-病原体互作”、“内吞作用”、“甘氨酸、丝氨酸和苏氨酸代谢”和“光合生物中的碳固定”相关的通路，而在 MEblack 模块中，富集了与“内质网中蛋白质加工”、“植物-病原体互作”和“糖酵解/糖异生”相关的通路。特别是，编码效应受体的 Pti1 和 RPS2 以及参与水杨酸信号通路的 NPR1、TGA 和 PR1 基因在 HT 中显著上调，而在 HY 中则下调。这表明 HT 中效应触发的免疫反应更强，水杨酸信号通路在 HT 对 Psa 的防御反应中起关键作用。此外，我们还鉴定了其他一些重要基因，这些基因参与苯丙烷生物合成和 Ca2+ 内流，在 HT 中高度表达。综上所述，这些结果为阐明猕猴桃在 Psa 感染过程中的防御机制提供了重要信息。
