Plant cells under siege: plant immune system versus pathogen effectors
1Center for Sustainable Resource Science, RIKEN, 1-7-22 Suehiro-cho, Tsurumi, Yokohama, Kanagawa 230-0045 Japan.
Current Opinion in Plant Biology
|September 7, 2015
Summary
Pathogen effector proteins help microbes infect plants by reopening stomata and disabling plant defenses. This review covers how fungal, oomycete, and bacterial effectors function at different infection stages.
Area of Science:
- Plant pathology
- Molecular biology
- Microbial pathogenesis
Background:
- Pathogen effector proteins are crucial for successful plant infection.
- Effectors target plant immunity at various infection stages, including stomatal penetration, apoplast invasion, and intracellular defense.
- Salicylic acid (SA)-dependent immunity is a key plant defense pathway targeted by pathogens.
Purpose of the Study:
- To summarize recent findings on effector functions in plant-pathogen interactions.
- To highlight effector roles in stomatal opening, apoplastic invasion, and intracellular defense.
- To discuss host cell-specific responses and the need for spatiotemporal resolution in studying plant-pathogen interactions.
Main Methods:
- Literature review of recent findings on pathogen effector proteins.
- Analysis of effector functions across fungal, oomycete, and bacterial pathogens.
- Discussion of host immune responses and cellular interactions.
Main Results:
- Pathogen effectors manipulate plant immunity by reopening stomata and deploying apoplastic and cytosolic effectors.
- Effectors target key steps in the infection process, from entry to intracellular invasion.
- Diverse pathogen types (fungal, oomycete, bacterial) utilize effectors to overcome host defenses.
Conclusions:
- Effectors are essential virulence factors that enable pathogens to successfully infect plants.
- Understanding effector function is critical for developing strategies to control plant diseases.
- Further research with high spatial and temporal resolution is needed to fully elucidate plant-pathogen interactions.
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