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.