Wang Xiaojie, Li Yawei, Liu Yuanyuan, Zhang Dongle, Ni Min, Jia Bing, Heng Wei, Fang Zemin, Zhu Li-Wu, Liu Pu
School of Horticulture, Anhui Agricultural University, Hefei, China.
School of Life Sciences, Anhui University, Hefei, China.
Front Plant Sci. 2021 Nov 11;12:756330. doi: 10.3389/fpls.2021.756330. eCollection 2021.
Kiwifruit bacterial canker caused by pv. (), is an important disease of kiwifruit ( Lind.). Plant hormones may induce various secondary metabolites to resist pathogens via modulation of hormone-responsive transcription factors (TFs), as reported in past studies. In this study, we showed that JA accumulated in the susceptible cultivar 'Hongyang' but decreased in the resistant cultivar of var. 'Jinkui' in response to . Integrated transcriptomic and proteomic analyses were carried out using the resistant cultivar 'Jinkui'. A total of 5,045 differentially expressed genes (DEGs) and 1,681 differentially expressed proteins (DEPs) were identified after infection. Two pathways, 'plant hormone signal transduction' and 'phenylpropanoid biosynthesis,' were activated at the protein and transcript levels. In addition, a total of 27 R2R3-MYB transcription factors (TFs) were involved in the response to of 'Jinkui,' including the R2R3-MYB TF subgroup 4 gene , which was downregulated in 'Jinkui' but upregulated in 'Hongyang.' The promoter region of has a MeJA responsiveness -acting regulatory element (CRE). Transient expression of the gene in the leaves of 'Jinkui' induced infection. Together, these data suggest that acts as a repressor to regulate the response of kiwifruit to infection. Our work will help to unravel the processes of kiwifruit resistance to pathogens and will facilitate the development of varieties with resistance against bacterial pathogens.
由丁香假单胞菌猕猴桃致病变种（Pseudomonas syringae pv. actinidiae）引起的猕猴桃细菌性溃疡病，是猕猴桃（Actinidia Lind.）的一种重要病害。以往研究报道，植物激素可能通过调节激素响应转录因子（TFs）诱导各种次生代谢产物来抵抗病原体。在本研究中，我们发现茉莉酸（JA）在感病品种‘红阳’中积累，但在抗病品种‘金魁’中响应猕猴桃细菌性溃疡病菌（Psa）侵染而减少。利用抗病品种‘金魁’进行了转录组和蛋白质组的综合分析。在接种Psa后，共鉴定出5045个差异表达基因（DEGs）和1681个差异表达蛋白（DEPs）。‘植物激素信号转导’和‘苯丙烷生物合成’两条途径在蛋白质和转录水平上被激活。此外，共有27个R2R3-MYB转录因子（TFs）参与了‘金魁’对Psa的响应，其中包括R2R3-MYB TF亚组4基因MYB4，该基因在‘金魁’中下调，但在‘红阳’中上调。MYB4的启动子区域有一个茉莉酸甲酯（MeJA）响应顺式作用调控元件（CRE）。MYB4基因在‘金魁’叶片中的瞬时表达诱导了Psa感染。总之，这些数据表明MYB4作为一种阻遏物来调节猕猴桃对Psa感染的响应。我们的工作将有助于揭示猕猴桃抗病的过程，并将促进抗细菌病原体品种的培育。
