Plant Defences Against Pathogens

Spec Mapping — OCR H420 Module 4.1.1 — Communicable diseases, content statement on plant defences against pathogens: physical (passive and inducible) and chemical (active) defences (refer to the official OCR H420 specification document for exact wording). This lesson covers preformed structural barriers, induced cell-wall reinforcement, the chemical-defence repertoire (terpenoids, phenols, alkaloids, defensive proteins, hydrolytic enzymes), the pattern-recognition signalling that triggers induced defences, and the hypersensitive response.

Plants are rooted and immobile. They cannot run from pathogens, they have no adaptive immune system with somatically rearranged antigen receptors, and they have no specialised mobile immune cells. Yet they live continuously immersed in a community of bacteria, fungi, oomycetes, viruses and insect vectors, and almost every plant manages to survive almost every encounter. The plant immune system is cell-autonomous: every plant cell carries the full defensive repertoire and the receptors needed to detect invasion, and the response is coordinated through chemical signalling (reactive oxygen species, calcium, salicylic acid, jasmonic acid, ethylene) rather than through migrating immune cells. OCR specification 4.1.1 requires you to describe these physical and chemical defences and to recognise that many are inducible — produced only after the plant detects an invader.

Key Definitions:

• Callose — a polysaccharide (β-1,3-glucan with some β-1,6 branching) deposited between the cell wall and plasma membrane at sites of infection or wounding.
• Tylose — a balloon-like outgrowth of a xylem-adjacent parenchyma cell into a xylem vessel, physically blocking it and sealing off the infection at the cost of reduced water transport.
• Phytoalexin — a low-molecular-weight antimicrobial compound synthesised by a plant de novo in response to infection (not stored constitutively).
• PAMP — pathogen-associated molecular pattern, a conserved microbial molecule (bacterial flagellin, fungal chitin, oomycete glucans) detected by plant receptors.
• PRR — pattern recognition receptor, a plant-cell-surface kinase that detects PAMPs.
• Hypersensitive response (HR) — rapid, programmed death of infected cells, sacrificing them to deny biotrophic pathogens living host tissue.
• Systemic acquired resistance (SAR) — a salicylic-acid-mediated plant-wide upregulation of defence, triggered by a localised attack, that primes distant tissues for any subsequent infection.

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Physical (Passive) Defences

Physical defences are structures that are already in place before infection occurs. They form the first line of defence.

1. Bark

The outer layer of woody stems is a dead, corky, lignified tissue. It physically prevents entry of pathogens and many insects. Cork cells contain suberin — a waxy substance that also resists water loss and microbial attack.

2. Waxy Cuticle

A hydrophobic layer of cutin (a polyester of hydroxy and epoxy fatty acids) overlaid with epicuticular waxes covers the epidermis of leaves and young stems. Because most fungal and oomycete spores need a film of liquid water to germinate and most bacteria need an aqueous environment to invade, the cuticle provides a dry, chemically inert and mechanically tough barrier. Many pathogens (black sigatoka, rusts, the bacterial pathogens) consequently enter the leaf through stomata — the only gaps in this otherwise impermeable surface — and some plants close their stomata in response to PAMP detection, a recently-described defence response. The cuticle also resists herbivore feeding and shields the cell wall from UV damage.

3. Cell Walls

The cellulose cell wall is a mechanical barrier that pathogens must digest or burst through. Built from cellulose microfibrils embedded in a matrix of pectins (the middle lamella) and hemicelluloses, the primary cell wall is mechanically strong (the tensile strength of cellulose rivals steel on a per-mass basis) and chemically resistant. Lignification of the wall in older tissues — the impregnation of the wall with the phenolic polymer lignin, deposited from monolignols by laccase- and peroxidase-mediated radical coupling — makes the wall yet harder to digest. Lignin is the second most abundant biopolymer on Earth (after cellulose itself) and is essentially the chief reason most pathogens cannot penetrate woody tissue. Many pathogens consequently secrete cellulases, hemicellulases, pectinases and (in the most aggressive cases) ligninases to dissolve the wall. Plants respond to PAMP detection by reinforcing the wall at the infection site with additional lignin deposition and with cross-linking of cell-wall proteins (extensins) into a denser matrix.

4. Callose Deposition

On detecting an invader, plants rapidly synthesise callose (a β-1,3-glucan) and deposit it between the cell wall and plasma membrane at the point of attack. Callose plugs plasmodesmata (cytoplasmic connections between cells), preventing the pathogen from spreading cell-to-cell. Callose is especially important in defence against fungal hyphae and viruses.

5. Tylose Formation

In response to infection of the xylem, parenchyma cells next to the vessels swell and push into the vessel lumen, forming tyloses. These balloon-like outgrowths physically block the vessel, preventing the pathogen (and any toxins) spreading in the transpiration stream. However, this also cuts off water flow — a trade-off.

6. Wound Sealing

Damage to plant tissue is immediately sealed with a mixture of suberin, lignin and phenolic compounds. Suberin is a polyester of long-chain hydroxy fatty acids and glycerol, with embedded waxes — chemically related to cutin but characteristic of internal protective layers (the Casparian strip of root endodermis, the cork of bark) rather than aerial cuticle. The wound-sealing response is rapid (hours), often involves the production of a layer of new cells immediately beneath the wound (wound periderm), and prevents pathogens from entering through the breached cuticle and cell wall.

7. Stomatal Closure

A more recently-recognised inducible barrier is stomatal closure in response to PAMP detection. Bacterial pathogens such as Pseudomonas syringae enter the leaf primarily through stomata, and the plant has co-opted the same stomatal regulation system that controls water loss to also close stomata when bacterial flagellin or LPS is detected. Some bacteria fight back: P. syringae secretes the phytotoxin coronatine, which mimics jasmonic acid and forces stomata to re-open.

flowchart TD
    A[Pathogen lands on plant] --> B{Physical barrier?}
    B -->|Yes| C[Cuticle, bark, cell wall block entry]
    B -->|Breached| D[Cell recognises PAMPs]
    D --> E[Callose deposited at plasmodesmata]
    D --> F[Tyloses form in xylem]
    D --> G[Chemical defences produced]
    G --> H[Terpenoids]
    G --> I[Phenols]
    G --> J[Alkaloids]
    G --> K[Defensive proteins]
    G --> L[Chitinases]

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Chemical (Active) Defences

Chemical defences are produced in response to infection. Many plants also store antimicrobial compounds in vacuoles or specialised cells, ready to be released on wounding.

1. Terpenoids

Terpenoids are a diverse family of lipid-soluble compounds that give plants their characteristic scents (e.g., menthol in mint, camphor in camphor tree, limonene in citrus). Many terpenoids have antibacterial and antifungal activity. Conifers release terpenoid resins that trap insects and kill fungi.

2. Phenols

Phenolic compounds such as tannins inhibit fungal and bacterial enzymes. Tannins bind to proteins, denaturing them and inactivating digestive enzymes — this is why unripe fruits taste bitter and astringent. Phenols also reduce the palatability of plant tissue to herbivorous insects.

3. Alkaloids

Alkaloids are nitrogen-containing organic compounds with bitter tastes and potent biological effects. They deter herbivores and inhibit microbial growth. Well-known examples include nicotine (tobacco), caffeine (coffee, tea), morphine (opium poppy), quinine (cinchona bark) and strychnine (Strychnos). Many of these are used in human medicine.

4. Defensive Proteins

Plants produce a wide repertoire of antimicrobial proteins and peptides:

• Defensins — small (~5 kDa) cysteine-rich peptides with conserved disulfide-stabilised folds (the cysteine-stabilised α-helix/β-sheet motif); they disrupt microbial membranes through electrostatic interaction with anionic phospholipids. Plant defensins are evolutionarily related to insect defensins and to vertebrate β-defensins, all sharing a common ancestral antimicrobial peptide module.
• Pathogenesis-related (PR) proteins — a heterogeneous group induced by infection; many have hydrolytic activity (chitinases, β-1,3-glucanases) or are involved in cell-wall reinforcement (PR-10 proteins).
• Lectins — proteins that bind specific sugar residues on microbial surfaces; ricin (castor bean) and concanavalin A (jack bean) are the most famous examples, though they are also toxins useful for laboratory glycoprotein analysis. Wheat-germ agglutinin and similar lectins bind chitin and disrupt fungal hyphae.
• Protease inhibitors — small proteins that inhibit insect and microbial proteases; the Bowman–Birk inhibitors of soybean are the textbook example. By blocking pathogen proteolysis they limit pathogen feeding and reproduction.

5. Hydrolytic Enzymes

• Chitinases — break down chitin in fungal cell walls.
• β-1,3-glucanases — digest the glucan component of fungal walls.
• Proteases — degrade proteins produced by invading microbes.

These enzymes are often stored in vacuoles and released when the cell is damaged.

6. Phytoalexins

Many plants produce broad-spectrum antimicrobial compounds called phytoalexins specifically in response to infection. Phytoalexins are defined by their de novo synthesis after infection rather than constitutive storage — they are induced compounds, not preformed defences. The defining concept dates from Müller and Börger's 1940 work on potato–Phytophthora interaction, in which they demonstrated that infected potato tissue acquired protection that could not be transferred chemically before infection — implying that a defence substance was synthesised in response to attack.

Examples of phytoalexins include:

• Rishitin and other terpenoid phytoalexins in potatoes — the original phytoalexin discovered by Müller and Börger.
• Camalexin in Arabidopsis thaliana — the laboratory-model plant and consequently the best-studied phytoalexin biosynthesis pathway.
• Medicarpin and related isoflavonoid phytoalexins in legumes (alfalfa, soybean).
• Resveratrol in grapes — the famous antioxidant found in red wine, originally a phytoalexin produced against Botrytis cinerea infection of grapes; the subject of intense (though contested) interest in human longevity research.
• Capsidiol in pepper and tobacco — a sesquiterpenoid phytoalexin.

Phytoalexin biosynthesis is energy-expensive, so plants synthesise them only when needed; concentrations rise from undetectable to fungicidal levels within hours of PAMP detection.

7. Antimicrobial cascade in response to infection

flowchart TD
    A[Pathogen lands on leaf surface] --> B{PAMP detected?}
    B -->|Flagellin, chitin, glucan| C[PRR binds PAMP]
    C --> D[ROS burst: H2O2, superoxide]
    C --> E[Ca2+ influx]
    D --> F[Callose plug at plasmodesmata]
    E --> G[Salicylic acid + jasmonic acid signalling]
    G --> H[PR proteins synthesised]
    G --> I[Phytoalexin synthesis]
    G --> J[Cell-wall lignification]
    H --> K[Chitinases, glucanases, defensins, lectins]
    I --> L[Camalexin, rishitin, resveratrol]
    F --> M[Spread limited]
    K --> M
    L --> M
    G --> N[Hypersensitive response: cell death]
    G --> O[Systemic acquired resistance: SA travels to distant leaves]

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Recognition of Pathogens — The Two-Tier Plant Immune System

How does a plant "know" it is being attacked? The conceptual framework — the two-tier plant immune system proposed by Jones and Dangl in 2006 — has revolutionised our understanding over the past two decades.