Defence Mechanisms in Plants PDF

# Defence Mechanisms in Plants ## Disease Resistance in Plants When a pathogen comes in contact with a host or enters into the host, it sometimes fails to develop a successful infection due to predominant defence mechanisms in the host. Majority of plants possess natural defence mechanisms to figh...

# Defence Mechanisms in Plants ## Disease Resistance in Plants When a pathogen comes in contact with a host or enters into the host, it sometimes fails to develop a successful infection due to predominant defence mechanisms in the host. Majority of plants possess natural defence mechanisms to fight against pathogens. This ability is under genetic control and inherited from generation to generations. This inherent capacity or ability of a host to defend against a pathogen or to restrict the establishment and subsequent activities of a potential pathogen is called **resistance**. Resistance is regarded as opposite of **susceptibility**. There are two main types of resistance: 1. **Horizontal (uniform) resistance:** General resistance in a given variety of plant spread evenly against all races (strains) of a pathogen is called horizontal resistance. This type of resistance is incomplete but permanent in nature. Such resistance is provided by a combination of lesser defence mechanisms and controlled by a group or groups of complementary genes (polygenic). 2. **Vertical (differential) resistance:** The resistance in a given variety of plant effective against some races (strains) of pathogen but not against others is called vertical resistance. It is complete but not permanent in nature. The vertical resistance is controlled by one gene (monogenic) or few genes (oligogenic) provided by one or a few defence mechanisms. ## Morphological or Structural Defence Mechanisms There are several morphological and structural barriers in host plants which restrict the entry of pathogen and subsequent establishment of infection. These barriers may be **pre-infectional** or passive (i.e. existing before infection) or **postinfectional** or active (i.e. formed after infection). ### Pre-existing Structural Defence 1. **Waxes and cuticles:** The cuticle layer present on the general plant surface consists of cutin and waxes. The cutin does not provide much resistance because of the presence of enzyme cutinases in some pathogens which degrade it. Cutin is usually penetrated by mechanical pushing. The waxes, on the other hand, provide greater resistance against the entry of pathogen. They act as principal defence structure in cuticle because no enzyme has been detected so far to be present in pathogen which can degrade it. The waxes are hydrophobic in nature which act as water repellent and prevent water drops to adhere on leaf surfaces. This also makes condition unfavorable for the growth of fungal pathogens. 2. **Structure of epidermal cell wall:** The external walls of epidermal cells form an important barrier for some pathogens due to thickness and toughness. The toughness of wall is mainly due to polymers of cellulose and hemicellulose. The lignification or deposition of silicic acid gives additional strength to the cell wall. Pyricularia orzyae, the causal organism of blast of rice, directly penetrates the epidermis through the motor cells and guard cells only because these cells are either not lignified or lignification takes place late. 3. **Structure and number of natural openings:** Many pathogens enter the host through natural openings such as stomata and lenticels and, therefore, the location, number and structure of these openings determine the pathogenicity of these pathogens. For example, small size of stoma surrounded by raised broad lipped structures found in Szinkum variety of Citrus and Mandarin oranges prevent entry of water drops containing bacteria – Xanthomonas citri, the causal organism of citrus canker. Some varieties of wheat open their stomata late in the day when moisture on leaf surface has dried. This prevents entry of germ tubes of Puccinia graminis tritici uredospores because up to that time the germ tubes become nonfunctional. Similarly, the lenticels having additional suberin layer, the hydathodes secreting concentrated liquid and nectaries with abundant hairs resist entry of pathogens. 4. **Internal structure:** Many internal structures such as thick inner wall of epidermal cells, presence of sclerenchymatous hypodermis in many stems, excessive leaf veins, etc., prevent the entry of many pathogens. For example, Pythium invades only juvenile tissues of seedlings. The secondary thickening prevents its entry. ### Post-infectional Structural Defence These defence structures develop in the host as a result of infection to prevent further spread of pathogen within the host. These include formation of cork layers, tyloses, abscission layers, swelling of cell walls and deposition of resins, gums, tannins, etc. 1. **Formation of cork layers:** Some pathogens stimulate the host to form multilayered cork cells below the area of infection. These develop as a result of stimulation of host cells by substances secreted by pathogen and prevent further invasion. Example, in *Prunus domestica* leaves attacked by *Coccomyces prunophorae*. 2. **Formation of tyloses:** The tyloses are formed by protrusion of cell walls of living cells through pits into the xylem vessels. These structures obstruct the movement of fluid in xylem vessels and at the same time obstruct the pathogen to spread further. In some varieties of sweet potato the tyloses are formed abundantly in the upper part of stem while the vascular wilt fungus – _Fusarium oxysporum_ f. sp. *batatas* still remains in the root and thus prevent further spread of the pathogens. 3. **Formation of abscission layer:** The abscission layer may be formed in response to activities of a pathogen (fungi, bacteria or virus). The abscission layer of such type is represented by an empty space between the healthy and diseased tissue formed due to dissolution of middle lamella. Due to this layer, the diseased portion separates and falls off. Example, shot hole disease of peach caused by *Clasterosporium carpophilum*. 4. **Deposition of gum:** The host deposits gum around the infected portion to form an impermeable border to restrict the pathogen. Examples, the rice varieties resistant to blast disease and Helminthosporium leaf-spot disease, restrict the pathogen by secreting and depositing gum by the adjoining cells. 5. **Swelling of cell walls and callus formation:** The cell walls of epidermal cells may swell and become lignified in contact with the appresorium and prevents further invasion. Sometimes divide and redivide to form a callus which encloses the intruding fungal hyphae to form a sheath. ## Biochemical Defence Mechanisms There are several chemical substances either present in the host before infection or produced after the infection to restrict the invasion by plant pathogen. Some biochemicals inactivate the pathogens or its toxins. ### Pre-existing Biochemical Defence 1. **Release of inhibitor compounds by plant in its environment:** Higher plants liberate gases as well as many organic chemicals into the atmosphere. The chemical substances exuded from phyllosphere and rhizosphere interact with the microflora and fauna around leaves and roots. Some of these chemicals promote the growth of microorganisms while others inhibit. They either directly inhibit the growth and activities of pathogens or promote the growth of some microorganism which function as antagonists of the pathogen. Some exudates provide nourishment to the antibiotic producing microflora so that the antibiotics produced by them inactivate the pathogenic microorganisms. Examples – The onion varieties in which the bulb scales are pigmented (red or yellow) are highly resistant to _Colletotrichum_ attack. It has been observed that the red scales of onion exude considerable quantities of water soluble phenolic compounds catechol and protocatechuic acid which prevent the spore germination of _Colletotrichum circinans_. (2) Some varieties of flax exude hydrocyanides (HCN) from the roots which are extremely toxic to wilt pathogen – _Fusarium axysporum_ f.sp. lini. Moreover, the chemical does not affect the growth of another microorganisms _Trichoderma_ spp. which are highly antagonistic to _Fusarium_. Marigold (_Tagetes erecta_) shows the presence of polyenes terthienyl and derivatives of bithienyl in the roots and root exudates which inhibit the pathogenic nematodes. Some varieties of gram (_Cicer arietinum_) secrete malic acid on the leaves which inhibits spore germination and hyphal growth of blight fungus. 2. **Presence of toxic chemicals in plant cells:** Cells of resistant hosts show the presence of higher amounts of toxic chemical substances. These anti-microbial substances include phenols, saponins, sulphur containing compounds, unsaturated lactones, cyanogenic glycosides, etc. Examples – (1) Some resistant varieties of potato contain higher amounts of chlorogenic acid in the periderm. This phenol becomes toxic to scab organisms – _Streptomyces scabies_ and wilt organism – _Verticillium albo-atrum_, (2) Tannic acid (a phenol) present in tobacco plants inhibits infection of tobacco mosaic virus, (3) Toxic terpenoid aldehydes present in the epidermal cells of cotton plants restrict the entry of pathogens, etc. 3. **Absence of essential nutrients for growth of pathogens:** Many facultative saprophytes and obligate parasites require the presence of available nutrients in the host for their growth and development. Absence of specific nutrients make the host plants resistant for such pathogens. Example the fungus _Rhizoctonia solani_ forms hyphal cushion and appresoria only on the susceptible hosts (radish, lettuce, etc.). It fails to produce appresorium in pure culture medium. However, if extracts of susceptible host is mixed in culture medium, it develops appresoria. 4. **Absence of common antigen:** The animal body produces antibodies against any foreign protein (antigen) introduced into it and protect the animal from the disease. Such antibodies are not formed in plants, but in some cases antigens common to antigens of pathogen exist in susceptible hosts such as some linseed plants contain antigens of _Melampsora lini_ (the causal organism of linseed rust) and cotton plants contain antigens of _Xanthomonas malvacearum_ (the causal organism of angular leaf spot disease). If the antigens common to pathogen are not present in a host, it becomes resistant to that particular pathogen. ### Post-infectional Biochemical Defence 1. **Release of phenols from non-toxic glucosides:** After the infection some pathogens help in the release of toxic phenols which move towards the site of infection. For example, in case of resistant variety of apple when infected with scab organism – _Venturia inaequalis_, β-glycosidase is produced. This enzyme acts on glucoside phloridzin to release phloretin and glucose. Phloretin is then oxidized by enzyme phenol oxidase to a toxic phenol-quinone which acts against the pathogen. Similar observations have been observed in case of fire blight disease of pears caused by _Erwinia amylovora_, leaf spot disease of rice caused by _Helminthosporium_, etc. 2. **Synthesis of phenols:** It has been observed in case of many diseases that the level of phenolic compounds increases in response to infection. Examples – (1) In cotton plants infected by _Verticillium_, the concentration of phenolic compounds increases in the roots and stems; (2) Increase in the level of phenol in resistant varieties of cabbage infected by _Botrytis cinerea_, etc. 3. **Phytoalexins:** Certain phenolic compounds which do not exist in the host or in the pathogen but synthesized after infection or due to mechanical or chemical injury. Such substances are called phytoalexins. The term phytoalexins (phyton = plant and alexin = warding off compounds) was coined by Muller and Borger (1940). All these compounds are mostly phenolic in nature except ipomeamarone. Kuc in 1972 defined phytoalexins as "antibiotics produced in plant pathogen interactions or as a response to injury or other physiological stimuli". They are produced by induction caused by any physical or chemical injury and by microorganisms such as fungi, bacteria and viruses. The quantity of phytoalexin biosynthesis is influenced by age of the host, concentration of inoculum, temperature and aeration. The phytoalexins inhibit the development of pathogens in general and fungal pathogens in particular. However, it has been observed that they are more toxic to nonpathogens than to pathogens. Some of the important phytoalexins are listed below :- 1. Pisatin is produced in Pisum sativum infected by Monilina fructicola. 2. Phaseolin is produced in Phaseolus vulgaris infected by Sclerotinia fructigena. 3. Cicerin is associated with blight of gram (Cicer arietinum) caused by Ascochyta rabie. 4. Rishitin is associated with late blight of potato caused by Phytophthora infestans. 5. Gossypol is reported from cotton (Gossypium) infected by Verticillium albo-atrum and Rhizopus nigricans. 6. Orchinol is formed by the interaction of Rhizoctonia repens with Orchis militaris tuber. 7. Ipomeamarone is produced in sweet potato (Ipomea batata) infected with Ceratocystis fimbriata causing black rot. 8. Isocoumarin is produced in carrot (Daucas carota) inoculated with a fungus non pathogenic to carrot – Ceratocystis fimbriata. 9. Medicarpin is produced in alfalfa (Medicago lupulina) inoculated with many pathogenic and non pathogenic fungi such as Helminthosporium turcicum, Colletotrichum phomoides, Stemphyllium loti, etc. 10. Defence by detoxification of toxins: Some resistant varieties of plants develop mechanism to neutralize the toxins produced by pathogen. For example, fusaric acid is metabolized and converted to nontoxic compound by resistant cotton and tomato plants. 11. Defence through induced synthesis of proteins and enzymes: Many resistant varieties of host plants synthesize proteins and enzymes to interact with pathogenic and non- pathogenic invadors. For example, sweet potato tissues infected with Ceratocystis fimbriata, the causal organism of black rot disease, produce ethylene which moves out to adjoining healthy tissue and alters their protein synthesis and enzyme activities. ### Defence through growth substances Some resistant varieties of host plants increase the level of auxin in response to infection. Auxins inhibit the actions of fungi. Similarly other growth substances such as gibberellins, cytokinins, ethylene, etc., also play important role in disease resistance. For example, the late blight of potato has been controlled by auxins, kinetin solution prevents the growth of powdery mildew on Cucumber leaves. ### Defence through inactivation of pathogen enzymes Many resistant varieties of host plants modify the substrates of pathogen enzymes. Several phenolic compounds are known to inactivate the enzymes of fungi. The calcium ions accumulated around the infected area caused by Rhizoctonia inhibit the activity of pathogen enzyme – polygalacturonase and prevent tissue maceration. ### Defence through altered respiration Certain resistant varieties increase the rate of cellular respiration following the infection. This accelerates the general metabolism of host and develops resistance. ### Defence through hypersensitive reaction Hypersensitive or necrogenous reactions usually occur in resistant host plant cells when an obligate parasite or a potent pathogen tries to establish parasitic relationship with the host. As soon as the pathogen comes in physiological contact with the hypersensitive host, the host cells at the site of invading pathogen are killed. During this process the nuclei of adjoining cells move towards the pathogen and disorganise to form brown grannules in the cytoplasm. Finally the adjoining cells are killed forming a trap of necrotic (dead) cells so that the pathogen fails to invade further. The toxic substances (usually phenols such as quinones) and hydrolytic enzymes (lyases) released from dead host cells (due to loss in cell permeability) may either kill the pathogen or restrict its further growth. Killing of the small part of the plant tissue results in a minor or local lesion. The size and extent of lesions depends on the ability of resistance of the host against invading pathogen. More resistant varieties of hosts produce smaller lesions whereas the less resistant varieties produce larger lesions. Hypersensitive reactions have been observed in wart disease of potato caused by Synchytrium endobioticum, blast of rice caused by Pyricularia orzyzae, late blight of potato caused by Phytophthora infestans and in many rusts, powdery mildews and viral diseases.