Fungus Derived Indole‐3‐Acetic Acid Controls Developmental Conidial Death in Magnaporthe oryzae

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.