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β-氨基丁酸通过抑制生物钟相关蛋白1激活桃果实中的水杨酸信号系统获得性抗性。

β-Aminobutyric acid activates SA-signalling systemic acquired resistance in peach fruit by suppressing the circadian clock associated protein1.

作者信息

Li Chunhong, Xia Yijia, Xiang Fei, Cao Shifeng, Zhou Minghua, Wang Kaituo, Zou Yanyu, Li Meilin, Zheng Yonghua

机构信息

College of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing 404000, People's Republic of China.

College of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing 404000, People's Republic of China; Institute of Fruit Function and Disease Management, Department of Public Health and Management, Chongqing Three Gorges Medical College, Chongqing 404000, People's Republic of China.

出版信息

Int J Biol Macromol. 2025 Apr;300:140040. doi: 10.1016/j.ijbiomac.2025.140040. Epub 2025 Jan 17.

DOI:10.1016/j.ijbiomac.2025.140040
PMID:39828166
Abstract

Circadian clock regulates plant development and physiology by anticipating daily environmental changes. Here we studied the core clock protein involved in β-aminobutyric acid (BABA)-inducible systemic acquired resistance (SAR) resistance to Rhizopus stolonifer in peach fruit. BABA elicitation barely primed the accumulation of jasmonate or ethylene, whose regulation was associated with morning-loop gene expression. Notably, BABA-induced resistance depended on the upregulation of salicylic acid (SA) signalling, accompanied by increased transcription of specific evening-loop genes. Through Y2H screening, pull-down and co-IP analyses, CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), a morning-expressed clock protein repressed by BABA, was identified as an interacting partner of NPR1 in regulating SA-dependent SAR. A CUT&Tag analysis indicated that the association of CCA1 with its target genes, which are enriched in EE or CBS motifs, was involved in SA pathway. Furthermore, EMSA, DLR, Y3H and Co-ip assays suggested that CCA1 did not directly affect the expression of SA-inducible genes but instead hindered the interaction between NPR1 and TGA1. Overexpression of PpCCA1 attenuated the transcription of SA-responsive PR genes, while mutation of PpCCA1 elevated these expressions. Collectively, PpCCA1 functions as a negative regulator of NPR1-dependent SA signalling through antagonistic crosstalk with the NPR1-TGA1 system, but BABA activates SAR by suppressing PpCCA1 in peach fruit.

摘要

生物钟通过预测日常环境变化来调节植物的发育和生理过程。在此,我们研究了参与桃果实中β-氨基丁酸(BABA)诱导的系统获得性抗性(SAR)以抵抗匍枝根霉的核心生物钟蛋白。BABA诱导几乎不会引发茉莉酸或乙烯的积累,其调节与晨环基因表达相关。值得注意的是,BABA诱导的抗性依赖于水杨酸(SA)信号的上调,同时伴随着特定夜环基因转录的增加。通过酵母双杂交筛选、下拉和免疫共沉淀分析,昼夜节律相关蛋白1(CCA1),一种受BABA抑制的晨表达生物钟蛋白,被鉴定为在调节SA依赖的SAR中NPR1的相互作用伴侣。切割与标签分析表明,CCA1与其富含EE或CBS基序的靶基因的结合参与了SA途径。此外,电泳迁移率变动分析、双荧光素酶报告基因检测、酵母三杂交和免疫共沉淀分析表明,CCA1不会直接影响SA诱导基因的表达,而是阻碍了NPR1与TGA1之间的相互作用。过表达PpCCA1会减弱SA响应PR基因的转录,而PpCCA1突变则会提高这些基因的表达。总体而言,PpCCA1通过与NPR1-TGA1系统的拮抗串扰作用作为NPR1依赖的SA信号的负调节因子,但BABA通过抑制桃果实中的PpCCA1来激活SAR。

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