Plant Defence Mechanisms — Quick Notes

Plant–Pathogen Relationships

  • Five potential relationships between plants and pathogens:

    • No relationship

    • Mutual adjustment between the plant and the pathogen

    • Plant is antagonistic to the pathogen

    • Pathogen is antagonistic to the plant

    • Mutual antagonism between the plant and the pathogen

  • Pathogen types mentioned: biotrophs and necrotrophs

Defense Overview

  • Passive defences: pre-existing barriers that protect the plant

  • Active defences: induced responses that enhance resistance

  • Distinction into rapid vs delayed responses (rapid responses occur quickly; delayed responses develop over time)

Passive Defences

  • Physical barriers: wax, cuticle, cell wall, stomata, lenticels

  • Chemical/other barriers (rapid/preformed):

    • Nutrient deprivation

    • pH adjustments

    • Phytoanticipins

    • Plant defensins

    • Membrane function (baseline protection)

Active Defences

  • Rapid responses: oxidative burst, reinforcement of membranes, early pathogen containment

  • Delayed responses: more robust defenses including cell wall reinforcement, hypersensitive cell death, phytoalexin accumulation, pathogenesis-related proteins, and systemic acquired resistance

Hypersensitive Response (HR) and Related Events

  • HR: localized programmed cell death at infection site to limit pathogen spread

  • Sequence (incompatible interactions):

    • Recognition of pathogen by host and formation of haustorium(a specialized structure in parasitic plants and fungi that penetrates the host's tissues to absorb water and nutrients) by the pathogen

    • Localized necrosis (the premature death of cells and living tissue, often caused by injury, infection, or lack of blood flow ) around infection site

    • Accumulation of inhibitory compounds and cellular changes to restrict growth

  • HR is a hallmark of effective local resistance against incompatible pathogens

Appressorium, Tylose, and Xylem Defense

  • Appressorium: fungal structure used to penetrate epidermal cells

  • Tylose (tyloses): plant-produced outgrowths that block xylem vessels to restrict pathogen spread

  • Lignituber: lignified tissue that reinforces barriers

  • In successful defence, advancing hyphae are blocked at the xylem vessel wall by tyloses/lignituber

Phases of Hyphal Interaction with Xylem

  • Pathogen attempts to penetrate xylem; defense structures impede progression within vascular tissue

  • Outcome: containment of infection and reduced systemic spread

Phytoalexins (Induced Antimicrobial Compounds)

  • Definition: antimicrobial compounds synthesized de novo in response to infection

  • Major classes and examples (selected):

    • Phenolic phytoalexins: chlorogenic acid, pisatin, phaseollin, scoparone, gossypol

    • Terpenoid phytoalexins: capsidiol, rishitin, ipomeamarone, glyceollins, medicarpin

    • Stilbenes: resveratrol

    • Indole-sulphur phytoalexins: camalexin

    • Others: brassinins, wy erone (illustrative examples in the table)

  • Role: inhibit pathogen growth and contribute to resistance

Elicitors, Receptors, and Defense Enzymes

  • Elicitors: molecules from pathogens that trigger plant defence responses

  • Receptors: located on the plasma membrane; detect elicitors and activate signaling

  • Defense enzymes involved in fungal cell-wall degradation:

    • Chitinase

    • β-1,3-glucanase

  • Role: break down fungal cell walls and release elicitors to amplify defense signaling

Cell Wall and Middle Lamella Defense

  • Pathogen attack often involves degradation of middle lamella

  • Plant enzymes (chitinase, glucanase) act to counteract fungal invasion and protect cell walls

Systemic Acquired Resistance (SAR) and Pathogenesis-Related (PR) Proteins

  • SAR: long-lasting, broad-spectrum resistance activated after an initial infection

  • PR proteins: accumulated as part of SAR; contribute to defense signaling and antimicrobial activity

Time Course of Defence Responses (Table 17.2)

  • Minutes: membrane depolarisation and electrolyte leakage

  • Hours: reactive oxygen generation; expression of genes for phytoalexin biosynthesis

  • Days: oxidative burst; membrane lipid peroxidation; rise in salicylic acid; cytoplasmic aggregation and HR cell death; phytoalexin accumulation

  • Subsequent: cell wall reinforcements; accumulation of PR proteins; systemic acquired resistance

Quick Reference – Key Concepts

  • Pathogen–plant interactions vary; plants possess both physical and chemical barriers

  • HR provides rapid, localized containment; SAR provides long-term, systemic protection

  • Phytoalexins and PR proteins are central to induced resistance

  • Enzymes like chitinase and glucanase actively counter fungal pathogens

  • Recognition of elicitors and signaling events trigger the defence cascade

Note on notation: Some measurements and terms appear with units or time points (e.g., phaseollin concentration and time after inoculation). Where applicable, these can be represented as: Phaseollin concentration (in extμg/extinoculatedsiteext{μg}/ ext{inoculated site}) and time axis t<br>ightarrowtext(h)t<br>ightarrow t ext{ (h)} to aid quick recall.