Plant Defense Mechanisms Against Infection

How Do Plants Defend Against Infection?

Introduction

• Presented by Dr. Sera Choi, Plant Breeding Institute, Camden Campus.

• IMMU2X11 Immunobiology Lecture 16.

Potato Late Blight

• Caused by Phytophthora infestans.

• Significant historical impact: Irish Famine.

• Irish population:

  • 1844: 8.4 million

  • 1851: 6.6 million

  • Resulted in 1 million deaths and 1 million emigrations.

• Key figures in understanding the disease: M.J. Berkeley and Anton de Bary.

Overview

1. Definition of host, pathogen, and disease interaction.

2. Classical plant host-pathogen interaction: gene-for-gene interaction.

3. Effector-Triggered Immunity (ETI).

4. Pattern-Triggered Immunity (PTI).

5. Two-layered plant immune system and the zig-zag model.

Host, Pathogen, and Disease Interaction

• Host:

  • Susceptible: Prone to disease.

  • Resistant: Able to withstand disease.

• Pathogen:

  • Virulent: Capable of causing disease.

  • Avirulent: Not capable of causing disease.

• Host-Pathogen Interaction:

  • Compatible: Leads to disease.

  • Incompatible: No disease.

• Disease Outcome:

  • Disease: Occurs when the interaction is compatible.

  • No Disease: Occurs when the interaction is incompatible.

Genetic Basis of Host-Pathogen Interaction: The Gene-for-Gene Hypothesis

• Developed by H.H. Flor, studying flax rust disease (Melampsora lini).

• Concept: For each resistance (R) gene in the host, there is a corresponding avirulence (Avr) gene in the pathogen.

• Host Genotype Example:

  • Host 1: Resistant to Pathotype 1.

  • Host 2: Susceptible to Pathotype 1.

  • F2 population ratio of Host 1 x Host 2: 3:1, indicating a single dominant allele (R) is responsible for resistance.

• Pathogen Genotype Example:

  • Pathotype 1: Avirulent to Host 1.

  • Pathotype 2: Virulent to Host 1.

  • F2 population ratio of Path 1 x Path 2: 3:1, indicating a single dominant allele (A, Avr) is responsible for avirulence.

• Genetic Cross Example:

  • Host: F1 gamete (R, r) x F1 gamete (R, r)

    • Resulting genotypes: RR, Rr, rr.

  • Pathogen: F1 gamete (A, a) x F1 gamete (A, a)

    • Resulting genotypes: AA, Aa, aa.

Gene-for-Gene Hypothesis: Protein Interactions

• Incompatible Interaction (No Disease):

  • Presence of both R1 protein in the host and Avr1 protein in the pathogen.

  • R1 protein recognizes Avr1 protein, triggering a defense response.

• Compatible Interaction (Disease):

  • Absence of either R1 protein or Avr1 protein.

  • If the plant has rl (lowercase r), it does not produce the R1 protein.

  • If the pathogen has avr1 (lowercase avr), it does not produce the Avr1 protein.

Effector-Triggered Immunity (ETI)

• Based on the gene-for-gene hypothesis.

• Effectors (Avrs): Pathogen-derived molecules that trigger immunity.

• R proteins: Plant resistance proteins that recognize effectors, leading to Effector-Triggered Immunity (ETI).

Plant Resistance Protein Structure

• Most discovered plant resistance proteins are NLR (nucleotide-binding leucine-rich-repeat) proteins.

• Domains: RPW8, NBARC, Variable N-terminal, LRR.

• Share structural similarity with proteins involved in animal immunity.

NLR Protein Types

• TNL (Toll-interleukin-1 receptor-like-NLR).

• CNL (Coiled-coil-NLR).

• RNL (RPW8-like-NLR).

Plant NLR Effector Recognition Strategies

1. Direct Recognition:

   • NLR directly binds to the effector.

   • Example: Sr35-AvrSr35; where Sr35 (NLR) directly interacts with AvrSr35 (Avr).

2. Indirect Recognition:

   • NLR recognizes a modified host target.

   • Example: RPS2-RIN4-AvrRpt2.

     • Normally, RIN4 is non-active.

     • AvrRpt2 cleaves RIN4, which activates RPS2 (NLR) and triggers immune responses.

3. Integrated Decoy:

   • NLR contains an integrated domain that mimics a host target.

   • Example: RRS1-PopP2.

     • RRS1 (NLR) contains a WRKY domain that mimics a transcription factor target.

     • PopP2 (Avr) targets the WRKY domain, leading to its capture and activation of immune responses.

Pattern-Triggered Immunity (PTI)

• Provides broad resistance against conserved pathogen-derived motifs.

• Experiment Example: Parsley cells exposed to pathogen extract trigger defense responses.

• Something non-invasive triggers immune response at the plant plasma membrane.

• Ligand (pep13) released from glycoprotein directly binds to membrane-bound receptor.

Structure of Pattern-Recognition Receptors (PRRs)

• Receptor-like Kinase (RLK) and Receptor-like Protein (RLP).

• Domains: LRR (Leucine-rich repeat), TM (Transmembrane domain), KD (Kinase domain).

PTI Activation

• PAMPs/MAMPs (Pathogen/Microbe-Associated Molecular Patterns) bind to PRRs.

  • Examples: flagellin, EF-Tu, chitin.

• Activation mechanism involves ligand binding on the LRR domain.

• Well-conserved among many PRR-PAMP perception events compared to ETI perception.

Plant Defense Systems: PTI and ETI

• Plants use two layers of immune recognition systems.

• PTI: Triggered by PRRs recognizing PAMPs.

  • Occurs in every cell due to the lack of a mobile immune cell system in plants.

  • Triggers responses like Ca2+ influx, reactive oxygen burst, callose deposition, defense gene activation, MAPK cascade, and phytohormone production.

• ETI: Triggered by NLRs recognizing effectors.

  • Leads to the Hypersensitive Response (HR), resulting in amplified and rapid immune responses that overlap with PTI responses.

The Zig-Zag Model

• Describes the endless arms race between host and pathogen.

• Phases:

  • PTI: Activated by PAMPs.

  • Effector-Triggered Susceptibility (ETS): Pathogen effectors suppress PTI.

  • ETI: Activated by NLRs recognizing effectors (Avr-R).

  • The cycle repeats as pathogens evolve new effectors.

  • $Amplitude \space of \space Defence \space increases \space as \space we \space move \space from \space PTI \space to \space ETI$

  • $Threshold \space for \space HR= Hypersensitive \space response$

  • $Threshold \space for \space effective \space resistance \space increases \space from \space left \space to \space right$

Plant Immune Response Pathways

• Pathogen perception via PRR and R proteins activates numerous immune outputs.

• These include changes in gene expression, phytohormone regulations, production of antimicrobial compounds and signaling molecules, ion exchange regulation, and cell-to-cell communication.

• $PAMP= Pathogen \space Associated \space Molecular \space Pattern$

Complexity of Plant Immune Signaling

• Plant immune signaling is complex, tightly regulated, and coordinated.

• Plants rely on an innate immune system without an adaptive system.

• They possess an extensive repertoire of immune receptors compared to animals.

• The host-pathogen arms race continuously adds complexity.

Boosting Resistance to Infections in Plants

• Further research is needed to understand how to enhance plant resistance to infections.