ArticleCellular microbiology2010
The Pseudomonas syringae type III effector HopG1 targets mitochondria, alters plant development and suppresses plant innate immunity.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 125 citations in OpenAlex.
- Pathogen effector tactics to suppress plant endomembrane system.Frontiers in plant science · 2026Review
- The flavonoid metabolic pathway genes Ac4CL1, Ac4CL3 and AcHCT1 positively regulate the kiwifruit immune response to Pseudomonas syringae pv. actinidiae.Plant molecular biology · 2025Article
- A Ralstonia solanacearum type III effector alters the actin and microtubule cytoskeleton to promote bacterial virulence in plants.PLoS pathogens · 2024Article
- Photorespiratory Metabolism and Its Regulatory Links to Plant Defence Against Pathogens.International journal of molecular sciences · 2024Review
- A conserved oomycete effector RxLR23 triggers plant defense responses by targeting ERD15La to release NbNAC68.Nature communications · 2024Article
- It takes two to tango: Plant hosts influence bacterial effector function through post-translational modifications.The Plant cell · 2024Article
- Heat-induced SUMOylation differentially affects bacterial effectors in plant cells.The Plant cell · 2024Article
- Involvement of oxidative stress in localization of bacterial spot infection in pepper plants.Journal of biosciences · 2024Article
- Exogenous melatonin mediates radish (Frontiers in plant science · 2023Article
- Review
- Fungal Effectoromics: A World in Constant Evolution.International journal of molecular sciences · 2022Review
- Metabolism and Signaling of Plant Mitochondria in Adaptation to Environmental Stresses.International journal of molecular sciences · 2022Review
- Maintenance of tRNA and elongation factors supports T3SS proteins translational elongations in pathogenic bacteria during nutrient starvation.Cell & bioscience · 2022Article
- The Pseudomonas syringae type III effector HopG1 triggers necrotic cell death that is attenuated by AtNHR2B.Scientific reports · 2022Article
- RIR1 represses plant immunity by interacting with mitochondrial complex I subunit in rice.Molecular plant pathology · 2022Article
- In planta transcriptomics reveals conflicts between pattern-triggered immunity and the AlgU sigma factor regulon.PloS one · 2022Article
- Regulation of theMicroorganisms · 2021Review
- What the Wild Things Do: Mechanisms of Plant Host Manipulation by Bacterial Type III-Secreted Effector Proteins.Microorganisms · 2021Review
- ThemSphere · 2021Article
- Leaping into the Unknown World ofJournal of fungi (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The bacterial plant pathogen Pseudomonas syringae uses a type III protein secretion system to inject type III effectors into plant cells. Primary targets of these effectors appear to be effector-triggered immunity (ETI) and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). The type III effector HopG1 is a suppressor of ETI that is broadly conserved in bacterial plant pathogens. Here we show that HopG1 from P. syringae pv. tomato DC3000 also suppresses PTI. Interestingly, HopG1 localizes to plant mitochondria, suggesting that its suppression of innate immunity may be linked to a perturbation of mitochondrial function. While HopG1 possesses no obvious mitochondrial signal peptide, its N-terminal two-thirds was sufficient for mitochondrial localization. A HopG1-GFP fusion lacking HopG1's N-terminal 13 amino acids was not localized to the mitochondria reflecting the importance of the N-terminus for targeting. Constitutive expression of HopG1 in Arabidopsis thaliana, Nicotiana tabacum (tobacco) and Lycopersicon esculentum (tomato) dramatically alters plant development resulting in dwarfism, increased branching and infertility. Constitutive expression of HopG1 in planta leads to reduced respiration rates and an increased basal level of reactive oxygen species. These findings suggest that HopG1's target is mitochondrial and that effector/target interaction promotes disease by disrupting mitochondrial functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.