Diversified Regulation of Cytokinin Levels and Signaling During Botrytis cinerea Infection in Arabidopsis

• Published in: Frontiers in plant science 2021-02, Vol.12, p.584042-584042
• Main Authors: Li, Beibei, Wang, Ruolin, Wang, Shiya, Zhang, Jiang, Chang, Ling
• Format: Article
• Language: English
• Subjects: Botrytis cinerea; cytokinins; ethylene; hormonal crosstalk; jasmonic acid; plant immunity; Plant Science
• ISSN: 1664-462X; 1664-462X
• DOI: 10.3389/fpls.2021.584042

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 .