How Plants Defend Themselves

Two General Categories of Defense:

I. Structural Characteristics

II. Biochemical/Physiological Mechanisms

Defense can take the form of both the above & may differ according to age of the plant, environment, stress, etc.

I. Structural Defenses – 2 types

A. Pre-existing

B. Formed in Response to Infection

A. Pre-existing Defenses

1. Trichomes – hairs- may prevent pathogen from reaching cell surface; or reduce water retention.

2. Epicuticular waxes: difficult to penetrate- lessens wetability.

3. Cuticle: difficult to penetrate.

4. Guard cells: shape, density and size- may make it difficult for pathogens to enter. e.g. wheat rust – some only open late in the day when rust can only invade during night or early morning.

5. Thickness of outer wall – may prevent entry or spread of disease.

B. Structures formed in response to attack:

4 Types

1. Histological Defense Structures

a. Cork layers - inhibits further invasion; prevents spread of toxins; deprives tissue + pathogen of nutrition. Example 3A

b. Abscission layers - e.g. stone fruits. Cells die around the infected tissue isolating disease. Tissue eventually drops-out eliminating the pathogen. Example 3B

c. Tyloses – protrusion of protoplast of adjacent cell (to vessel) and formation of cell wall with lumen. Effectively blocks

pathogen from advancing through tissue. Example 3B

d. Gums – deposition of gums (carbohydrate/protein) in intercellular spaces. Forms an impenetrable barrier. Pathogen is isolated and dies. Common in stone fruit. Example 3C

3A

3B

3C

2. Cellular Defense Structures

- changes in the cell wall

- wall appositions/papillae

Response to attempted invasion very fast. Composed of:

a. Callose

b. Cellulose

c. Lignin – very resistant

- encasement – Haustoria are surrounded by papillae-like material

Wall Apposition

Wall Apposition

Haustorium

Encasement

Encasement

Encasement Composition

Callose and Cellulose

3. Cytoplasmic Defense Reaction?

weak pathogens – cytoplasm becomes granular & dense and structures appear (Peroxisomes) – mycelium dies and infection ceases.

4. Necrotic Reaction – hypersensitivity. 4a

a. Host is penetrated; pathogen contacts protoplast

b. Nucleus migrates to site, disintegrates, host cell dies.

c. Cell browns and pathogen dies obligate parasites, nematodes with bacteria – cell membranes are disrupted – cell death

Usually, pathogen is dependent on living tissue; thus disease is limited.

4A

II. Biochemical Defenses

- Defense much more dependent on biochemical/physiological properties than on structural.

A. Pre-existing

1. Inhibitors released into environment

Fungitoxic/Fungistatic compounds secreted on surface of leaves or incorporated in

waxes and cuticle.

Phenolic compounds – onion smudge

terpines - blue mold tobacco

2. Defense through lack of essential factors

a. Lack of recognition – fails to establish relationship between host/pathogen

b. Lack of sensitive sites for toxin

Pathogen produces poison which is not toxic to host

c. Lack of critical nutrient

eg. Pectobacteria (Erwinia) on potato – soft rot varieties of potato that have lots of sugar (less starch) are more susceptible

3. Inhibitors of growth and enzymes phenols and tannins

B. Induced Metabolic Defenses

1. Hypersensitive Reaction

Much-like necrotic reaction, but considerable faster – cells and some surrounding cells die. Accumulation of Phenols, Oxidized Phenols & Phytoalexins.

2. Increase Phenols

Lots of different Phenolic chemicals accumulate in cells and kill pathogens

OH

3. Phytoalexins – are toxic substances produced in appreciable quantities only after stimulation by pathogenic microorganisms, chemical or mechanical injury.

Most inhibit growth of fungi, but some are active against bacteria and nematodes. – Some are phenols

Stimulated by Elicitors

1. Cell was component – glucose

2. Heavy metal ions

3. Pathogen

May or may not cause resistance to disease.

4. Phenol – oxidizing enzymes

oxidize phenols to quinones; more toxic to microbes

5. Substrates resisting enzymes of the pathogen

Pectin is susceptible to enzymatic decay, but is more resistant if complexed with divalent cations (Ca or Mg)

Masceration - breaks cell apart by degrading pectin – less so with high Ca+2 or Mg+2 content

6. Fungitoxic Cyanide “Death Chamber”

HC N completed in wall linked by sugar molecule; when pathogen degrades wall release cyanide. Respiratory toxin.

7. Detoxification of Pathogen Toxins

Fungal toxins kill plant cells

Metabolized by host cell for resistance

8. Induced Resistance

Develops after pre-inoculation of plants w/various biotic agents or after pre-treatment with various chemical or physical agents.

It is non-specific since, regardless of the agent used as the inducer resistance is increased for a variety of pathogens.

Systemic Induced Resistance (SIR)

Infection is localized, after several days, plant is resistant to attack in other areas. Usually resistance is expressed as small local lesions or complete resistance (no symptoms).

b proteins – newly synthesized proteins found in hypersensitive Reaction.

But role in systemic induced resistance is unknown

Elector from cell wall is released, travels through plant and induced other plant defenses.

Such as phytoalexins

proteinase inhibitors

Polyphenoloxidase

Perioxidase

b proteins

or other compounds