All plants have resistance to some pathogens under cutin conditions. Different plants defend themselves against pathogens in different ways.
The defense mechanism of plants against pathogens falls into two categories: 1. Morphological or Structural Defense Mechanism 2. Biochemical Defense Mechanism.
1. Morphological or Structural Defense Mechanism:
The first line of defense against pathogens is the surface barriers which a pathogen must penetrate before it can caval infection. The entry of the pathogen may either be through the epidermal cell walls directly or through the natural openings in the epidermis, such as stomata, lenticels, hydathodes or through injured areas caused by living or non-living agencies.
Defense Structure Existing before Infection:
(a) Waxes and Cuticle:
The cuticle which consists of cutin and waxes forms the outermost covering of the epidermal cells and appears as a non-cellular, membranous layer. Waxes play a defensive role by forming hydrophobic surface which acts as a water repellent. The cuticle acts as a physical or chemical barrier to infection.
(b) Structure of Epidermal Cell Wall:
The thick and tough outer wall of epidermal cells forms an important barrier for certain pathogens. Lignification or the presence of silicic acid in the epidermis of some plants acts as an important structural defense mechanism.
(c) Structure of Natural Openings:
Most pathogens enter plants through natural openings. In case of the stem rust of wheat, the varieties in which stomata open late in the morning are resistant because the germ tubes of the spores germinating in the night dew desiccate. This is due to the evaporation of the dew before the stomata begin to open. This is called functional resistance.
(d) Internal Structural Barriers to Pathogen Invasion:
In certain varieties of wheat, the presence of bundles of increased areas of sclerenchyma cells prevents infection.
Defense Structures formed after Infection:
(a) Formation of Cork Layers:
In the Rhizoctonia disease of potato tubers, following infection, cork layers are produced just below the areas of infection. This layer prevents further invasion by the pathogens. It blocks the spread of toxic substances produced by the pathogen and checks the flow of nutrients and water from the healthy to the infected area and this result in the starvation of the pathogen.
(b) Formation of Tyloses:
Tyloses are the overgrowths of the protoplast of adjacent living parenchymatous cells which protrude into xylem vessels through half bordered pits. Tyloses are usually considered to be one of the factors which cause wilting. Tyloses in some varieties of sweet potato are formed abundantly and quickly, thus bring about resistance as this prevents the further spread of the pathogen.
(c) Formation of Abscission Layers:
Due to the formation of abscission layer in peach flower by the bacterium or fungus and in sour cherry trees due to infection with necrotic ring spot and other viruses, there is the swelling of the two layers of cells surrounding the infected spot. They become thin walled while the pectic substances of the middle lamella get dissolved resulting into the formation of abscission layers.
(d) Gum Deposition:
Gum deposition along the borders of diseased lesions often serves as a protective demarcation and constitutes a type of mechanical resistance.
2. Biochemical Defense Mechanism:
The biochemical defense mechanism may consist of the presence or absence of a particular chemical substance or group of substances in a host plant which interferes with the growth and multiplication of the pathogen.
The biochemical agent may be present before infection or may be produced by the interaction of the host and pathogen (post-infectional). This type of defense mechanism which involves the chemicals is called biochemical defense mechanism.
Pre-Existing Biochemical Defense Mechanism:
Inhibitors Released by the Plant:
The blight resistant varieties of Cicer have more glandular hairs which secrete malic acid on the leave than the susceptible varieties. High concentration of malic acid inhibits spores germination and retards the hyphal growth of the fungus.
Root exudates also protect plants against diseases. The root exudates from the resistant varieties of flax excrete a glucoside which produces hydrocyanic acid after hydrolysis which is inhibitory to the soil inhabitants.
Inhibitory Substances Present in the Plant Cell after Infection:
In potato scab causal by a bacterium Streptomyces scabies, higher concentration of chlorogenic acid have been reported in potato tubers. In citrus leaves isopimpinellin gives resistance against Glucosporium limetticola. Pears become resistance to fire blight due to the presence of phenolic glucoside arbutin.
Resistance to several fungal plant pathogens has been ascribed to higher concentration of fungitoxic phenolic substances and their oxidation products and to increased polyphenol oxidase (PPO) activity as a result of infection.
The activity of PPO seems to be important because it can oxidize phenolic compounds to quinones which may be more fungitoxic.
Aromatic substances such as polyphenols, phenolic glucosides, flavonoids, anthocyanins, aromatic amino acids, etc., accumulate in and around infected plant tissues.
The high concentrations of chlorogenic acid in the roots of certain potato varieties is supposed to be the main defense mechanism against the wilt pathogen called verticilium.
Absence of Nutrients Required by Pathogen:
Unless the host tissue provides required necessary nutrients for the proper growth of a pathogen the latter will not grow and cause infection. These growth factors may be vitamins, polypeptides, amino acids, enzymes, etc.
The pH of the plant tissue influences many physiological processes in both plants and pathogens (specifically enzymatic action). Thus pH sensitive pathogens are unable to show their effect on the plant.
Osmotic Pressure and Permeability Effects:
The cells of parasitic fungi usually have higher osmotic pressure than that of the host cells. In case of lettuce mildew, cells of resistant tissues or varieties have a higher osmotic pressure than those of the susceptible ones. Resistance can be modified by altering the mineral nutrition of the plant.
Defense through Absence of Common Antigens:
The idea that the antigens shared by the host and pathogen may determine the nature of disease reactions has been given by Doubly et. al.
The term phytoalexins was introduced by Muller and Boerger. They described them as the substances that inhibit fungus development formed when living plant tissues are invaded by a fungal parasite. Phytoalexins can also be described as antibiotics which arise from metabolic interactions of host pathogen. These are inhibitory to the microbes, insects, nematodes, etc., which attack the plants.
Several phytoalexins are as follows:
An abnormal tetrahydrofuran.
The chromocoumarin ring system and is phenolic ether.
Similar to pisatin, isolated from detached bean pods.
A phytoalexin associated with Ascomychota blight of gram. It has two fluorescent phenols.
It is a bicyclic non-sesquiterpene alcohol.
An antifungal compound isolated from Gossypium (cotton).
A sesquiterpene phytoalexin isolate from Capsicum (pepper).
Defense through Induced Synthesis of Proteins and Enzymes:
Induced synthesis of proteins and enzymes play an important role in resistance. In case of black rot of sweet potato the tissues inoculated with the pathogen (i.e., fungus Ceratocystis fimbrioata) and with the non-pathogen that induces immunity showed marked change in 9 of 13 enzymes.
Defense through Detoxification of Pathogen Toxin:
The toxin pircularins, chlorogenic acid detoxifies the piricularins when applied to rice seedings. Piricularin is also detoxified by ferulic acid which is oxidized by peroxidase. Its oxidized products are also able to detoxify piricularin.
Defense through Altered Respiration:
The relation of increased respiration to disease and susceptibility is unclear. In some incompatible combinations of host-pathogen (or resistant), the increase is initially greater than in compatible (susceptible) combinations of host – pathogen. It is due to altered respiration.