A multifaceted crosstalk between brassinosteroid and gibberellin regulates the resistance of cucumber to Phytophthora melonis

被引:0
作者
Kang, Yunyan [1 ]
Jiang, Zhongli [1 ]
Meng, Chen [1 ]
Ning, Xianpeng [1 ]
Pan, Gengzheng [1 ]
Yang, Xian [1 ]
Zhong, Min [1 ]
机构
[1] South China Agr Univ, Coll Hort, Guangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
brassinosteroids; gibberellin; cucumber; hormone interactions; Phytophthora melonis; AGE-RELATED RESISTANCE; DISEASE DEVELOPMENT; GENE-EXPRESSION; DEFENSE; IMMUNITY; GROWTH; BIOSYNTHESIS; INFECTION; RESPONSES; CAPSICI;
D O I
10.1111/tpj.16855
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Cucumber plants are highly susceptible to the hemibiotroph oomycete Phytophthora melonis. However, the mechanism of resistance to cucumber blight remains poorly understood. Here, we demonstrated that cucumber plants with impairment in the biosynthesis of brassinosteroids (BRs) or gibberellins (GAs) were more susceptible to P. melonis. By contrast, increasing levels of endogenous BRs or exogenously application of 24-epibrassinolide enhanced the resistance of cucumber plants against P. melonis. Furthermore, we found that both knockout and overexpression of the BR biosynthesis gene CYP85A1 reduced the endogenous GA(3) content compared with that of wild-type plants under the condition of inoculation with P. melonis, and the enhancement of disease resistance conferred by BR was inhibited in plants with silencing of the GA biosynthetic gene GA20ox1 or KAO. Together, these findings suggest that GA homeostasis is an essential factor mediating BRs-induced disease resistance. Moreover, BZR6, a key regulator of BR signaling, was found to physically interact with GA20ox1, thereby suppressing its transcription. Silencing of BZR6 promoted endogenous GA biosynthesis and compromised GA-mediated resistance. These findings reveal multifaceted crosstalk between BR and GA in response to pathogen infection, which can provide a new approach for genetically controlling P. melonis damage in cucumber production.
引用
收藏
页码:1353 / 1368
页数:16
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