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转录组分析表明,AcWRKY75转录因子降低了猕猴桃对 假单胞菌 的抗性。 (注:原文中“pv.”后面内容缺失,翻译按现有内容尽量完整呈现)

Transcriptome analysis revealed that AcWRKY75 transcription factor reduced the resistance of kiwifruit to pv. .

作者信息

Ye Lixia, Luo Minmin, Wang Yafang, Yu Mengqi, Wang Zhi, Bai Fuxi, Luo Xuan, Li Li, Huang Qiong, Peng Jue, Chen Qi, Chen Qinghong, Gao Lei, Zhang Lei

机构信息

Hubei Key Laboratory of Germplasm Innovation and Utilization of Fruit Trees, Institute of Fruit and Tea, Hubei Academy of Agricultural Science, Wuhan, China.

College of Horticulture and Gardening, Yangtze University, Jingzhou, China.

出版信息

Front Plant Sci. 2024 Oct 24;15:1488572. doi: 10.3389/fpls.2024.1488572. eCollection 2024.

Abstract

The kiwifruit canker disease caused by pv. (Psa) seriously threatens the development of kiwifruit industry. So far, only a limited number of Psa-resistant kiwifruit varieties have been identified, and the underlying molecular mechanisms are still largely unknown. In this study, we evaluated the Psa resistance of six hybrid populations and screened a resistant segregation population RF. Then, transcriptome analysis on the Psa extremely high-resistant (HR) and extremely high-susceptible (HS) plants of the RF population was performed. KEGG enrichment analysis revealed that differentially expressed genes (DEGs) were significantly enriched in plant hormone signal transduction pathways, including auxin, abscisic acid, zeatin, jasmonic acid and salicylic acid. Furthermore, several transcription factors (TFs), especially WRKY TFs, were identified among the DEGs. The qRT-PCR showed that was highly expressed in the HS plants. Additionally, was significantly induced in the HS cultivar 'Hongyang' after Psa inoculation. Sequence amplification analysis showed that there was polymorphism in the DNA sequence of gene, but no HR or HS-specific differences were observed. Subcellular localization and transcriptional activity analysis confirmed that AcWRKY75 functions as a nucleus-located transcriptional activator. Transient overexpression of in kiwifruit leaves reduced the resistance to Psa, while silencing by virus-induced gene silencing (VIGS) slightly enhanced the resistance to Psa. Furthermore, AcWRKY75 exhibited a weak interaction with the promoter of the ABA-related DEG (Acc27163). Our findings elucidated that AcWRKY75 may negatively regulate the Psa resistance of kiwifruit through the hormone signaling pathway, which laid a foundation for the analysis of the disease resistance mechanism of kiwifruit canker.

摘要

由丁香假单胞菌猕猴桃致病变种(Psa)引起的猕猴桃溃疡病严重威胁着猕猴桃产业的发展。到目前为止,仅鉴定出有限数量的抗Psa猕猴桃品种,其潜在分子机制仍 largely unknown。在本研究中,我们评估了六个杂交群体对Psa的抗性,并筛选出一个抗性分离群体RF。然后,对RF群体中Psa极高抗(HR)和极高感(HS)植株进行了转录组分析。KEGG富集分析表明,差异表达基因(DEGs)在植物激素信号转导途径中显著富集,包括生长素、脱落酸、玉米素、茉莉酸和水杨酸。此外,在DEGs中鉴定出了几个转录因子(TFs),尤其是WRKY TFs。qRT-PCR表明 在HS植株中高表达。此外,Psa接种后,HS品种‘红阳’中 被显著诱导。序列扩增分析表明, 基因的DNA序列存在多态性,但未观察到HR或HS特异性差异。亚细胞定位和转录活性分析证实,AcWRKY75作为一种定位于细胞核中的转录激活因子发挥作用。在猕猴桃叶片中瞬时过表达 降低了对Psa的抗性,而通过病毒诱导基因沉默(VIGS)沉默 则略微增强了对Psa的抗性。此外,AcWRKY75与ABA相关DEG (Acc27163)的启动子表现出弱相互作用。我们的研究结果阐明,AcWRKY75可能通过激素信号通路负调控猕猴桃对Psa的抗性,这为分析猕猴桃溃疡病的抗病机制奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1879/11540699/64f270966c33/fpls-15-1488572-g001.jpg

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