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The Plant Infection Test: Spray and Wound-Mediated Inoculation with the Plant Pathogen Magnaporthe Grisea
Published on: August 4, 2018
Fungus Derived Indole-3-Acetic Acid Controls Developmental Conidial Death in Magnaporthe oryzae
Yuming Ma1, Qiao Liu1, Qing Shen2
1State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangdong Provincial Key Laboratory of Microbial Signals and Disease Control, Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
Abstract:
Ferroptotic death of the developing conidia is important for pathogenicity of the blast fungus Magnaporthe oryzae, yet its regulatory mechanism is not fully elucidated in fungal cell. In this study, we found that elevated indole-3-acetic acid (IAA) promoted iron and lipid peroxide accumulation, leading to a higher degree of ferroptotic death of conidia. By characterising the IAA biosynthesis mutant, tam1Δ, we found that conidial death was positively correlated with levels of endogenous IAA. Furthermore, we found an IAA-dependent lipid metabolism gene mutant ppoaΔ displayed deficiencies in conidial death and the consequent delay in appressorium formation, and reduced pathogenicity. Exogenous addition of two types of phosphatidylethanolamines (PEs), DOPE and SLPE, could at least partially restore such defects in both tam1Δ and ppoaΔ, indicating that IAA promotes ferroptosis by affecting lipid metabolism and/or peroxidation. Additionally, we found TAM1 affected autophagy by modulating transcription of the ATG8 gene. Overall, our study reveals that M. oryzae produces and uses IAA to promote pathogenicity through triggering ferroptotic conidial death during pathogenic development. Our results provide a theoretical basis for blast disease control using IAA synthesis inhibitors.
Insights
The blast fungus Magnaporthe oryzae uses indole-3-acetic acid (IAA) to trigger ferroptotic conidial death, enhancing its pathogenicity. Inhibiting IAA synthesis offers a potential strategy for controlling rice blast disease.
Area of Science:
- Plant Pathology
- Mycology
- Molecular Biology
Background:
- Ferroptotic cell death in Magnaporthe oryzae conidia is crucial for pathogenicity.
- The precise regulatory mechanisms of ferroptosis in fungal cells remain unclear.
Purpose of the Study:
- To elucidate the role of indole-3-acetic acid (IAA) in regulating ferroptotic conidial death and pathogenicity in Magnaporthe oryzae.
- To investigate the molecular mechanisms underlying IAA-mediated ferroptosis.
Main Methods:
- Characterization of IAA biosynthesis mutant (tam1Δ) and lipid metabolism gene mutant (ppoaΔ).
- Analysis of iron and lipid peroxide accumulation, conidial death, and pathogenicity.
- Investigation of the effects of exogenous phosphatidylethanolamines (PEs) on mutant phenotypes.
- Assessment of TAM1's role in autophagy via ATG8 gene transcription modulation.
Main Results:
- Elevated IAA levels promoted iron and lipid peroxide accumulation, increasing ferroptotic death.
- The tam1Δ mutant showed reduced conidial death correlated with lower endogenous IAA.
- The ppoaΔ mutant exhibited defects in conidial death, delayed appressorium formation, and reduced pathogenicity.
- Exogenous DOPE and SLPE partially restored defects in tam1Δ and ppoaΔ mutants.
- TAM1 was found to modulate ATG8 gene transcription, affecting autophagy.
Conclusions:
- Magnaporthe oryzae utilizes IAA to promote pathogenicity by inducing ferroptotic conidial death.
- IAA influences fungal pathogenicity through lipid metabolism and peroxidation pathways.
- Inhibitors of IAA synthesis present a promising theoretical basis for managing rice blast disease.
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