ArticleRice (New York, N.Y.)2021
The Fungal Effector Avr-Pita Suppresses Innate Immunity by Increasing COX Activity in Rice Mitochondria.
Article in Rice (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Pathogenicity and virulence of the blast fungusVirulence · 2026Review
- The Moniliophthora roreri Effector MrB1 Affects Cellular Homeostasis and Induces Genotype-Dependent Necrosis in Theobroma cacao.Molecular plant pathology · 2026Article
- Blue light receptor phot2 collaborates with NRL-30 to negatively regulate immunity by reducing mitochondrial protein PRXIIF stability in potato.Molecular horticulture · 2026Article
- CgCFEM1 and CgCFEM2 modulate virulence in Colletotrichum gloeosporioides by integrated regulation of TOR and cAMP-PKA signaling pathways.BMC microbiology · 2026Article
- MDP25-VDAC3 Complex Orchestrates Actin Remodeling and Mitochondrial Dynamics to Modulate Innate Immunity in Arabidopsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MIRO1-mediated mitochondrial fusion is required for stomatal immunity in Arabidopsis.Nature plants · 2026Article
- Rice blast pathogen effector AvrPib compromises disease resistance by targeting Raf-like protein kinase OsMAPKKK72 to inhibit MAPK signaling.Journal of integrative plant biology · 2026Article
- Pathogen effector tactics to suppress plant endomembrane system.Frontiers in plant science · 2026Review
- Transposable elements create distinct genomic niches for effector evolution among Magnaporthe oryzae lineages.BMC biology · 2025Article
- Genome-Wide Characterization and Expression Pattern Analysis Insights into PlantInternational journal of molecular sciences · 2025Article
- Molecular Insights into Rice Immunity: Unveiling Mechanisms and Innovative Approaches to Combat Major Pathogens.Plants (Basel, Switzerland) · 2025Review
- The microRNA-encoded peptide miPEP398b regulates heat tolerance in grapevine.Plant physiology · 2025Article
- Status on Genetic Resistance to Rice Blast Disease in the Post-Genomic Era.Plants (Basel, Switzerland) · 2025Review
- Live cell imaging of plant infection provides new insight into the biology of pathogenesis by the rice blast fungus Magnaporthe oryzae.Journal of microscopy · 2025Review
- The Role of Genetic Resistance in Rice Disease Management.International journal of molecular sciences · 2025Review
- Rice E3 ubiquitin ligases: From key modulators of host immunity to potential breeding applications.Plant communications · 2024Review
- Article
- Fungal effectors: past, present, and future.Current opinion in microbiology · 2024Review
- The unconventional resistance protein PTR recognizes the Magnaporthe oryzae effector AVR-Pita in an allele-specific manner.Nature plants · 2024Article
- Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundAvr-Pita was the first effector identified in the blast fungus (Magnaporthe oryzae)-rice (Oryza sativa) pathosystem. However, the molecular mechanism underlying its effects on the host plant has remained a long-standing mystery.
resultsHere, we report that ectopically expressing Avr-Pita in rice enhances susceptibility to M. oryzae and suppresses pathogen-associated molecular pattern (PAMP)-triggered defense responses. Avr-Pita targets the host mitochondria and interacts with the cytochrome c oxidase (COX) assembly protein OsCOX11, a key regulator of mitochondrial reactive oxygen species (ROS) metabolism in rice. Overexpressing Avr-Pita or OsCOX11 increased COX activity and decreased ROS accumulation triggered by the fungal PAMP chitin. OsCOX11-overexpressing plants showed increased susceptibility to M. oryzae, whereas OsCOX11-knockdown plants showed resistance to M. oryzae.
conclusionsTaken together, these findings suggest that the fungal pathogen M. oryzae delivers the effector Avr-Pita to the host plant, where it enhances COX activity thus decreasing ROS accumulation. Therefore, this effector suppresses host innate immunity by perturbing ROS metabolism in the mitochondria.
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