The fungal pathogen Magnaporthe oryzae chemically disables the jasmonic acid (JA)-mediated defense signaling in rice.

M. oryzae secretes the antibiotic biosynthesis monooxygenase (Abm) and its endogenously produced chemical effector 12-hydroxy jasmonic acid (12OH-JA) in a biphasic manner to suppress host immunity during establishment of the blast disease in rice. Loss of Abm function leads to activation of the host defense via jasmonate signaling and consequently blocks fungal invasion in rice plants. Brownish orange inclusions depict the sites of methyl JA-induced innate immunity that blocks the abmΔ strain of M. oryzae in the first invaded rice cell. A, appressorium; C, conidium; IH, invasive hypha; JA-Ile, isoleucine conjugate of JA; Jaz9, jasmonate-ZIM domain repressor protein 9; MeJA, methyl JA; WT, wild-type M. oryzae. Hypothetical receptors or transporters for the fungal JA derivatives have been depicted on the host cell surface. The schematic has not been drawn to scale.

Abm-Based hydroxylation of endogenous JA by M. oryzae overcomes the innate immunity in rice. 

Schematic representation of the single hydroxylation event that governs successful colonization of rice tissue by the blast fungus. The pathogenicity gene cluster encodes a monooxygenase, Abm, which converts endogenous JA into 12OH-JA in the WT M. oryzae and is utilized to disable the host innate immunity. Loss of Abm leads to accumulation of fungal MeJA, which triggers the host innate immunity and restricts the growth of the abmΔ M. oryzae in the first invaded rice cell.

Working model for the role of ATS in M. oryzae pathogenesis.
(A) Schematic representation of accumulation of ATS (ABC3 Transporter Substrate), in the wild type or abc3Δ appressoria, affecting host entry. (B) The figure illustrates a proposed crosstalk/mechanistic link between ATS accumulation and ion homeostasis, Tef2-function, and F-actin dynamics during M. oryzae pathogenesis.