Unit 5: Mechanisms of Pathogenesis in Plant Pathogens

1. Types of Parasitism and Variability in Plant Pathogens

1.1 Types of Parasitism

Parasitism is a symbiotic relationship where one organism (the parasite) lives on or within another organism (the host) and derives nutrients at the host's expense. In plant pathology, pathogens are classified based on their nutritional mode and dependence on the host.

Classification based on Mode of Nutrition

• Biotrophs: Pathogens that derive nutrients from living host cells. They establish a specialized feeding structure (haustoria) and do not kill the host cells rapidly, as they require a living host to complete their life cycle.
  • Examples: Rusts (Puccinia), Powdery mildews (Erysiphe), Viruses.
• Necrotrophs: Pathogens that kill host cells (usually via toxins or enzymes) and utilize the contents of the dead cells for nutrition.
  • Examples: Botrytis cinerea (Gray mold), Soft rot bacteria (Pectobacterium).
• Hemibiotrophs: Pathogens that start their infection cycle as biotrophs (living on live tissue) but switch to a necrotrophic mode (killing tissue) in later stages.
  • Examples: Phytophthora infestans (Late blight), Colletotrichum species.

Classification based on Dependency

• Obligate Parasites: organisms that can grow and reproduce only on living hosts. They cannot be cultured on artificial nutrient media.
  • Examples: Viruses, Downy mildews, Powdery mildews.
• Facultative Saprophytes: Organisms that are ordinarily parasites but can survive as saprophytes (living on dead organic matter) for a part of their life cycle.
  • Examples: Smut fungi (Ustilago).
• Facultative Parasites: Organisms that are ordinarily saprophytes but can become parasitic under favorable conditions.
  • Examples: Pythium, Rhizoctonia.

1.2 Variability in Plant Pathogens

Pathogens are not static; they evolve to overcome host resistance and environmental stresses.

Mechanisms of Variability in Fungi

1. Mutation: A sudden, heritable change in the nucleotide sequence of DNA. While most mutations are deleterious, some confer virulence or fungicide resistance.
2. Sexual Reproduction (Recombination): Meiotic division allows for the reassortment of genes, creating new genotypes. This occurs in the perfect stage (teleomorph) of fungi.
3. Heterokaryosis: The presence of genetically different nuclei within the same mycelium or spore. This results from the fusion (anastomosis) of hyphae from different strains.
4. Parasexualism: A mechanism in imperfect fungi (which lack a sexual cycle) where genetic recombination occurs via the fusion of haploid nuclei, followed by mitotic crossing over and haploidization.

Mechanisms of Variability in Bacteria

1. Conjugation: Transfer of plasmid DNA (often containing virulence factors) from a donor to a recipient bacterium through a pilus.
2. Transformation: Uptake of free genetic material from the environment (e.g., from lysed bacterial cells) and incorporation into the genome.
3. Transduction: Transfer of genetic material from one bacterium to another via a bacteriophage (virus).

Specialized Terms

• Physiological Race: A subgroup within a species of pathogen that can be distinguished from others only by its virulence on specific differential host cultivars.
• Biotype: A subdivision of a physiologic race.

2. Role of Enzymes in Pathogenesis

Enzymes are large protein molecules that catalyze chemical reactions. Pathogens secrete extracellular enzymes to penetrate physical barriers (cuticle, cell wall) and break down host tissues for nutrients.

2.1 Constitutive vs. Inducible Enzymes

• Constitutive Enzymes: Produced by the pathogen continuously, regardless of the presence of the substrate (host tissue). Essential for initial penetration.
• Inducible Enzymes: Produced only when the specific substrate (e.g., pectin, cellulose) is detected in the environment.

2.2 Key Enzyme Groups

A. Cutinases

• Target: Cutin (the main component of the plant cuticle).
• Function: Cutinases are esterases that break the ester linkages in cutin molecules.
• Significance: Many fungi (e.g., Fusarium solani f.sp. pisi) secrete cutinase to breach the cuticle directly.

B. Pectinases (Pectolytic Enzymes)

• Target: Pectin (the main component of the middle lamella, which acts as the "cement" holding plant cells together).
• Types:
  • Pectin Methylesterases (PME): Remove methyl groups from pectin chains.
  • Polygalacturonases (PG): Hydrolyze the glycosidic bonds between galacturonic acid units (chain splitting).
  • Pectin Lyases (PL): Cleave pectin chains via trans-elimination.
• Significance: These are the primary enzymes involved in Soft Rot diseases. They cause tissue maceration (separation of cells) leading to mushy, watery decay.

C. Cellulases

• Target: Cellulose (the structural framework of the plant cell wall).
• Mechanism: Cellulose breakdown requires a multi-enzyme complex (C1, Cx, and -glucosidase) to convert insoluble cellulose into glucose.
• Significance: Crucial for the softening of cell walls and nutrient release in rots and blights.

D. Hemicellulases

• Target: Hemicellulose (xylans, galactans).
• Examples: Xylanase, Arabinase.
• Significance: Necessary because hemicellulose links cellulose fibers to pectin, creating a rigid wall structure.

E. Ligninases

• Target: Lignin (the most resistant component, found in woody tissues).
• Examples: Lignin peroxidase, Laccase.
• Significance: Primarily produced by Basidiomycetes (wood-rotting fungi like White Rot).

3. Toxins in Pathogenesis

Toxins are non-enzymatic metabolites produced by pathogens that injure host cells at very low concentrations. They may act directly on protoplasts, alter membrane permeability, or inhibit specific metabolic enzymes.

3.1 Classification of Toxins

A. Host-Specific Toxins (HST) / Pathotoxins

These toxins are selectively toxic only to the host plants susceptible to the pathogen producing them. They are determinants of pathogenicity (if the pathogen loses the toxin, it loses the ability to cause disease).

• Victorin (HV-toxin):
  • Pathogen: Cochliobolus victoriae (formerly Helminthosporium victoriae).
  • Host: Oats (specifically variety 'Victoria').
  • Action: Causes severe leaf blight and root rot.
• T-Toxin:
  • Pathogen: Cochliobolus heterostrophus (Race T).
  • Host: Corn with Texas Male Sterile (TMS) cytoplasm.
  • Action: Targets mitochondria, inhibiting respiration and causing Southern Corn Leaf Blight.
• HC-Toxin:
  • Pathogen: Cochliobolus carbonum.
  • Host: Corn.

B. Non-Host-Specific Toxins (NHST)

These toxins affect a wide range of plant species, not just the specific host of the pathogen. They act as virulence factors (they increase the severity of the disease but are not strictly required for infection).

• Tabtoxin (Wildfire Toxin):
  • Pathogen: Pseudomonas syringae pv. tabaci.
  • Host: Tobacco.
  • Action: The toxin is hydrolyzed in the plant to release tabtoxinine--lactam, which inhibits the enzyme glutamine synthetase. This leads to ammonia accumulation and characteristic chlorotic halos.
• Tentoxin:
  • Pathogen: Alternaria alternata.
  • Action: Inhibits chloroplast development, causing chlorosis (yellowing) in seedlings.
• Fusaric Acid:
  • Pathogen: Fusarium species (wilt pathogens).
  • Action: Increases cell membrane permeability and chelates metal ions, contributing to wilt symptoms.

4. Growth Regulators in Disease Development

Pathogens can alter the hormonal balance of the plant by either producing growth regulators themselves or inducing the plant to produce/inhibit them. This imbalance leads to symptoms like hypertrophy (cell enlargement), hyperplasia (cell division), stunting, or defoliation.

4.1 Auxins (Indole-3-Acetic Acid / IAA)

• Normal Function: Cell elongation, differentiation, apical dominance.
• Pathological Role:
  • Pathogens induce high levels of IAA, leading to uncontrolled cell division (hyperplasia) and enlargement (hypertrophy).
  • Prevents cell wall lignification, keeping tissues soft for pathogen invasion.
• Disease Examples:
  • Crown Gall (Agrobacterium tumefaciens): The bacterium transfers T-DNA into the plant genome, which codes for constitutive auxin (and cytokinin) production, resulting in tumor formation.
  • Olive Knot (Pseudomonas savastanoi): Bacteria produce IAA causing galls.

4.2 Gibberellins

• Normal Function: Stem elongation, seed germination.
• Pathological Role: Excess production leads to abnormal elongation (etiolation).
• Disease Examples:
  • Bakanae Disease of Rice (Gibberella fujikuroi): The fungus produces high levels of gibberellin. Infected plants grow much taller and thinner than healthy plants ("Foolish Seedling" disease) and are often sterile.

4.3 Cytokinins

• Normal Function: Cell division, prevention of senescence.
• Pathological Role:
  • Inhibition of senescence leads to "Green Islands" (spots of green tissue surrounding an infection site on a yellowing leaf), common in rusts and mildews.
  • Breaking of apical dominance leads to "Witches' Broom" (proliferation of lateral shoots).
• Disease Examples:
  • Fasciation (Corynebacterium fascians): Causes leafy galls due to cytokinin imbalance.
  • Witches' Broom of Cacao (Moniliophthora perniciosa).

4.4 Ethylene

• Normal Function: Fruit ripening, senescence, leaf abscission.
• Pathological Role:
  • Pathogen stress triggers "Stress Ethylene" production by the plant.
  • Causes Epinasty (downward curling of leaf petioles), premature yellowing (chlorosis), and defoliation.
• Disease Examples:
  • Common in vascular wilts caused by Ralstonia solanacearum and Fusarium oxysporum. It causes the characteristic drooping of leaves even when water is available.

4.5 Abscisic Acid (ABA)

• Normal Function: Growth inhibition, stomatal closure, dormancy.
• Pathological Role:
  • Pathogens may induce ABA to close stomata (limiting gas exchange) or inhibit growth causing stunting.
• Disease Examples:
  • Stunting in viral diseases (e.g., Cucumber Mosaic Virus) is often associated with elevated ABA levels.