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Plant bio

Plant/pathogen interactions

QuestionAnswer
Why are most plants resistant to most pathogens? • High biodiversity • Plant pathogen co-evolution • Isolation of disease through natural barriers • Changing environmental conditions
Why in agricultural settings are plants more prone to disease? • Low biodiversity (monocultures) • No co-evolution between plant and pathogen • No isolation through natural barriers • Human-altered environmental conditions
What organisms cause plant disease? Fungi Nematodes Oomycetes Viruses Bacteria
What's the biggest problem? Major crop loss
Which diseases cause crop loss? Blast disease/smut disease (fungus)
The disease triangle predicts the likelihood of disease occurring Plants are exposed to countless microbes, but few of these interactions lead to disease - why? - host must be susceptible - pathogen can avoid host defences - environment must favour the pathogen
What factors reduce the likelihood of disease? Resistant plants, little/no pathogens and a non-conductive environment
What is plant immunity based upon? - pathogen recognition and defence - no adaptive immunity in plants
What are the parts of the plant immune system? First branch: defenses outside of the plant cell Second branch: defenses inside of the plant cell
First branch Pattern-Triggered immunity (PTI) recognizes pathogens outside of the plant cell MAMPs/DAMPs are pathogen molecules which are detected by PRRs Plant cell surface receptors (PRRs) detect pathogen presence
Many plant PRR extracellular receptors have three domains 1) extracellular leucine-rich repeat domain that recognizes conserved microbial elements 2) a transmembrane domain 3) intracellular kinase domain
MAMPs are recognized by specific PRRs ie. FLS2 - flagellin
Plants respond to pathogens with large-scale transcriptional changes Defence responses include: • Increased synthesis of stress hormones • Synthesis of antimicrobial compounds • Production of reactive oxygen species (ROS) • Production of callose
Biotechnology and plant PRRs in disease resistance breeding The PRR EFR is not present in tomato EFR confers resistance to bacterial blight Introducing EFR from Arabidopsis (another plant) into tomato confers resistance to bacterial blight
Second branch - ETI (effector triggered immunity)
Pathogens produce effectors that enhance their virulence • Effectors are small molecules secreted by pathogens, that facilitate infection and colonization of the host plant • Effectors can be proteins, small RNAs, or other types of molecules, and they often target specific host proteins or cellular processes
NLRs – intracellular immune receptor which recognize pathogen effectors - NLRs recognize effectors intracellularly Defense responses include: • Calcium ion influx • Production of reactive oxygen species (ROS)
Plant NLRs typically consist of three domains - signal transduction ie. TIR - ON/OFF switch ie. NB-ARC - pathogen recognition ie. LRR
Active NLRs can form "resistosomes" which result in Calcium influx and cell death pathogen effectors - NLR activation - resistosome formatin
Biotechnology and plant NLRs in disease resistance breeding NLR from wild potato confers resistance to late blight in cultivated potato NLR- = no growth NLR+ = growth
Zig zag model Pathogen MAMPs are recognized by PRRs PTI - (first branch) Pathogen effectors suppress defence response Pathogen effectors are recognized by plant NLRs ETI - (second branch)
Red queen hypothesis Species must constantly adapt and co-evolve to remain competitive
Intracellular NLRs - highly diverse immune system components - highly variable across all plants - many genomic events contribute to the high variability of NLRs
Too much diversity in immune receptors? - can result in plant autoimmunity and mismatching immune receptors
Created by: reub8n
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