Opposing effects of MYZUS PERSICAE-INDUCED LIPASE 1 and jasmonic acid influence the outcome of Arabidopsis thaliana–Fusarium graminearum interaction

Authors

• Syeda T. Alam, University of North Texas
• Sujon Sarowar, University of North Texas
• Hossain A. Mondal, University of North Texas
• Ragiba Makandar, University of North Texas
• Zulkarnain Chowdhury, University of North Texas
• Joe Louis, University of Nebraska - LincolnFollow
• Jyoti Shah, University of North TexasFollow

ORCID IDs

Jyoti Shah https://orcid.org/0000-0002-5604-1771

Document Type

Article

Date of this Version

2022

Citation

Mol Plant Pathol. 2022;23:1141–1153.

DOI: 10.1111/mpp.13216

Comments

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial- NoDerivs License

Abstract

Fusarium graminearum (Fg) is an important fungal pathogen of small grain cereals that can also infect Arabidopsis thaliana. In Arabidopsis, jasmonic acid (JA) signalling involving JASMONATE RESISTANT 1 (JAR1), which synthesizes JA-isoleucine, a signalling form of JA, promotes susceptibility to Fg. Here we show that Arabidopsis MYZUS PERSICAE-INDUCED LIPASE 1 (MPL1), via its influence on limiting JA accumulation, restricts Fg infection. MPL1 expression was up-regulated in response to Fg infection, and MPL1-OE plants, which overexpress MPL1, exhibited enhanced resistance against Fg. In comparison, disease severity was higher on the mpl1 mutant than the wild type. JA content was lower in MPL1-OE and higher in mpl1 than in the wild type, indicating that MPL1 limits JA accumulation. Pharmacological experiments confirmed the importance of MPL1-determined restriction of JA accumulation on curtailment of Fg infection. Methyl-JA application attenuated the MPL1-OE- conferred resistance, while the JA biosynthesis inhibitor ibuprofen enhanced resistance in mpl1. Also, the JA biosynthesis-defective opr3 mutant was epistatic to mpl1, resulting in enhanced resistance in mpl1 opr3 plants. In comparison, JAR1 was not essential for the mpl1-conferred susceptibility to Fg. Considering that methyl-JA promotes Fg growth in culture, we suggest that in part MPL1 curtails disease by limiting the availability of a plant-derived Fg growth-promoting factor.