Transcriptomic analysis reveals that cell wall- and hypersensitive response (HR)-related genes are involved in the responses of apple to Valsa mali

被引:8
|
作者
Wang, Chao [1 ]
Mao, Xia [1 ]
Zhao, Dan [1 ]
Yu, Hongqiang [1 ]
Duo, Hu [1 ]
Sun, E. [1 ]
Lu, Yuan [1 ]
Zuo, Cunwu [1 ,2 ]
机构
[1] Gansu Agr Univ, Coll Hort, Lanzhou 730070, Peoples R China
[2] Key Lab Crop Sci Arid Environm Gansu Prov, Lanzhou 730070, Peoples R China
基金
中国国家自然科学基金;
关键词
Gene expression profiles; Apple; Valsa mali; Cell wall; Hypersensitive response; ARABIDOPSIS TCH4; SALICYLIC-ACID; RESISTANCE; CANKER; EXPRESSION; INFECTION; INSIGHTS; PROVIDES; KINASES;
D O I
10.1007/s11816-022-00763-z
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The necrotrophic pathogen Valsa mali (Vm) resulting Valsa canker of apple is considered one of the most destructing fungal diseases. To study the resistance mechanism, we investigated gene expression profiles of suspension cells from resistant varieties 'Dongbeishanjingzi' (DS, Malus baccata) and susceptible varieties 'Gala' (GL, Malus x domestica) in response to Vm metabolism (VmM) using RNA sequencing (RNA-seq). Functional enrichment showed that differentially expressed genes (DEGs) were widely involved in multiple metabolisms or signals, such as "Lipid metabolic process", "plant hormone signal transduction" and "plant-pathogen interaction". Further expressional patterns exhibited that induction of genes related to ''xyloglucan biosynthetic process'' and ''cell wall biogenesis'' was beneficial for cell wall integrity and tolerance of DS cells. In brassinosteroid signaling, we identified that TCH4 gene MbTCH4-1 positively regulated Vm resistance of 'Fuji' fruit, but BSK gene MdBSK1 negatively regulated the resistance. In contrast, cell death associated with hypersensitive response caused by up-regulation of CNGCs and CDPK genes is an important cause of weakened tolerance in GL cells. Our results provide a new insight direction for the molecular mechanism of apple against Valsa canker.
引用
收藏
页码:539 / 551
页数:13
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