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Understanding Plant Pathogen Interactions
Oct 28, 2024
Plant Pathogen Interaction
Overview
Discussion on plant-pathogen interaction and how pathogens interact with plant cells.
Proteins and Factors in Interaction
Plant Cell:
PRR (Pattern Recognition Receptors)
: Located on the plant cell surface.
Pathogen:
PAMP/MAMP (Pathogen/Microbe Associated Molecular Pattern)
: Recognized by plant's PRR.
Effector Molecules/Pathogen Effectors
: Detected by plant cell's R protein.
Plant Immunity Types
ETI (Effector Triggered Immunity):
Evoked by pathogen effectors.
PTI (Pattern/PAMP Triggered Immunity):
Triggered by PAMP/MAMP.
Plant Pathogen Interaction Details
PRR-PAMP Binding:
PRR molecules on the plant cell bind to PAMP molecules on the pathogen.
Triggers PTI, initiating the MAPK cascade and activation of defense genes.
Pathogen Effector Detection:
Pathogens secrete effector molecules to hijack plant cells.
NBLRR Proteins (Nucleotide-Binding Leucine-Rich Repeat):
Detect pathogen effectors and belong to the R protein class.
Activation of R genes causes ion flux (efflux of hydroxide, potassium ions, and influx of calcium, hydrogen ions).
Results in HR (Hypersensitive Response) leading to oxidative burst, ROS production, and lignin/callos deposition to prevent infection spread.
Short-term and Long-term Responses
Hypersensitive Response (HR):
Short-term containment of pathogen infection.
Induces SAR (Systemic Acquired Resistance), a more advanced immunity.
Activates transcription of proteins like phytoalexins and chitinases to degrade fungal cell walls and affect orthopod exoskeletons.
Hormonal Signaling Pathways
Different pathways activated based on pathogen type:
Necrotrophic Pathogen:
Induces JA (Jasmonic Acid) pathway.
Biotropic Pathogen:
Induces SA (Salicylic Acid) pathway.
Activation of these pathways induces PR gene transcription for defense.
Conclusion
PR gene expresses PR protein (e.g., chitinases) to combat pathogen infection.
Overview of how plant immune systems respond to pathogen encounters.
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