Li Beibei, Wang Ruolin, Wang Shiya, Zhang Jiang, Chang Ling
State Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, China.
School of Biology and Agricultural Resources, Huanggang Normal University, Huanggang, China.
Front Plant Sci. 2021 Feb 10;12:584042. doi: 10.3389/fpls.2021.584042. eCollection 2021.
Cytokinins (CKs) can modulate plant immunity to various pathogens, but how CKs are involved in plant defense responses to the necrotrophic pathogen is still unknown. Here, we found that infection induced transcriptional changes in multiple genes involved in the biosynthesis, degradation, and signaling of CKs, as well as their contents, in pathogen-infected leaves. Among the CKs, the gene expression of () was remarkably induced in the local infected leaves and the distant leaves of the same plant without pathogen inoculation. -zeatin (Z) and its riboside (ZR) accumulated considerably in infected leaves, suggesting an important role of the -zeatin type of CKs in the plant response to . Cytokinin double-receptor mutants were more susceptible to infection, whereas an exogenous CK treatment enhanced the expression levels of defense-related genes and of jasmonic acid (JA) and ethylene (ET), but not salicylic acid (SA), resulting in higher resistance of to . Investigation of CK responses to infection in the JA biosynthesis mutant, , and ET-insensitive mutant, , showed that CK signaling and levels of CKs, namely, those of isopentenyladenine (iP), isopentenyladenine riboside (iPR), and -zeatin (Z), were enhanced in -infected leaves. By contrast, reductions in iP, iPR, Z, and Z riboside (ZR) as well as ZR contents occurred in -infected leaves, whose transcript levels of CK signaling genes were likewise differentially regulated. The () gene was upregulated in infected leaves of whereas another type-A response regulator, , was significantly downregulated, suggesting the existence of a complex regulation of CK signaling via the ET pathway. Accumulation of the -zeatin type of CKs in -infected leaves depended on ET but not JA pathways. Collectively, our findings provide evidence that CK responds to infection in a variety of ways that are differently modulated by JA and ET pathways in .
细胞分裂素（CKs）可调节植物对多种病原体的免疫，但CKs如何参与植物对坏死营养型病原体的防御反应仍不清楚。在此，我们发现病原体感染会诱导感染叶片中多个参与CKs生物合成、降解和信号传导的基因及其含量发生转录变化。在CKs中，（）的基因表达在局部感染叶片和同一植株未接种病原体的远处叶片中显著诱导。玉米素（Z）及其核糖苷（ZR）在感染叶片中大量积累，表明玉米素型CKs在植物对的反应中起重要作用。细胞分裂素双受体突变体对感染更敏感，而外源CK处理增强了防御相关基因以及茉莉酸（JA）和乙烯（ET）的表达水平，但不影响水杨酸（SA），从而导致对的抗性增强。对JA生物合成突变体和ET不敏感突变体中CK对感染的反应研究表明，感染叶片中CK信号传导和CKs水平，即异戊烯腺嘌呤（iP）、异戊烯腺嘌呤核糖苷（iPR）和玉米素（Z）的水平增强。相比之下，感染叶片中iP、iPR、Z和Z核糖苷（ZR）以及ZR含量降低，其CK信号传导基因的转录水平也受到不同调节。（）基因在感染叶片中上调，而另一种A型反应调节因子则显著下调，表明通过ET途径存在对CK信号传导的复杂调节。感染叶片中玉米素型CKs的积累依赖于ET途径而非JA途径。总的来说，我们的研究结果提供了证据，表明CK以多种方式对感染作出反应，这些方式在中受到JA和ET途径的不同调节。
