Defence Mechanism in Plants- Phase I

Sanjeet Kumar
Ravenshaw University
sanjeet.biotech@gmail.com

Defence Mechanism in Plants

The relation of host and parasite provides an excellent example of struggle for existence. Two entities, the parasite and the host compete each other by all means at their disposal, one to gain access and establishment and other to keep away the parasites or at least making it harmless by neutralizing its menacing efforts. The battle is long and strategist succeeds. Plants and their pathogens have evolved together. In course of their long coexhistance plants possessing features, that enabled them to escape or restrict pathogenic infection, have survived. Time to time such features are being regularly added to the plant arsenal through mutation, hybridization etc. This inherent potential of a plant to defend against pathogen or to limit the establishment and subsequent undesirable activities of potential pathogen is called resistance. The mode of defence in different plant is quite variable against pathogens. Each kind of plant reacts to defend itself in its own characteristic manner against each of the various pathogens that attack it. Thus resistance and susceptibility of a plant are heritable traits whose expressivity is largly governed by prevailing environmental conditions during infection.

Defence mechanism in plants may be broadly discussed under two heads:

1.     Structural or morphological defence mechanism.

2.     Biochemical defence mechanism.

STRUCTURAL DEFENCE MECHANISM

Microscopically visible structural characterstics present on the surface or within the healthy plant tissue acting as physical barrier that prevent pathogen from penetration or spread within the host may be:-

a)     Pre- existing or passive

b)    Post – inflectional or active

Pre-existing structural defence: Presence of structural barriers in plants without prior contact with the pathogen that create hindrance in infection include, amount and quality of wax & cuticle, the structure of the epidermis cell wall, the size shape and location of stomata and lenticels and presence of thick walled mechanical tissues.

Wax and Cuticle:

The cuticle is membranous noncellular layer present as outer covering on epidermal cells. It contains cutin and wax and regarded as a principal obstacle to entry of the pathogen within host. Cuticular thickness has been linked with host resistance especially in those cases in which pathogen usually enter into the host by direct penetration, exerting mechanical pressure on the host surface. The susceptibility of young plant tissues has been attributed to its uneven and thin cuticle. Cuticular waxes, on the other hand provide greater resistance against penetration by pathogen, as no enzyme of pathogenic origin is known that can degrade it. Cuticular waxes are long chain aliphatic compounds, hydrophobic in nature that act as water repellent and reduce the adherence of water on the leaf surface. Thus it creates a condition unfavourable for the growth of the pathogen.

Structure of Epidermal Cell Wall:

The thickness and toughness of the outer epidermal cell wall are impotant characteristics that provide resistance in some plnts against certain pathogen. Polymers of cellulose and hemicelluloses impart toughness in the cell wall. The lignifications or deposition to salicic acid on the walls of epidermis, provides additional resistance to the cell wall. In rice leaves, deposition of salicic acid on lignocelluloses wall of epedremis is known to increase the resistance against rice blast fungus,Pyricularia oryzae . Here main entry point of the fungus is, through motor cells that remains unlignified longer than other epidermal cells. Tough epidermal layer apart from resisting invasion, additionally may prevent an established pathogen from breaking out of the host tissue and liberating its infective propagules and consequently reducing the amount of inoculums production and spread of the disease.

Structure of Natural openings:

Many fungal and bacterial pathogen prefer natural openings like stomata, lenticels etc. for their entrance within the host. Thus the location, number, structure and mode of such openings, amy determine the pathogenicity of the several pathogens. For instance Puccinia graminis, the stem rust of wheat pathogen can enter the host, only when stomata are open. In some rust resistant wheat varieties, stomata remain closed much of time and open quite late in the day. As a result, by the time stomata opens, the infecting structures produced by germinating uredospore, on the surface of leaves in the night dew, dries out due to evaporation of the moisture. The stomatal structure is also known to provide effective resistance to certain hosts against some of their pathogens. In canker resistant Mandarin orange variety, presence of very narrow slit like stomatal openings, surrounded by broad lipped structure that project over and nearly covers the stoma, prevents entry of water drops that may contain citrus canker causing bacterial pathogen Xanthomonas citri from initiating infection. Similarly, the size and internal structure of lenticels has a direct bearing on the host resistance. Apple varieties having large lenticels on the fruit surface are easily accessable by Pseudomonas populosum,  the apple spot diseases bacterium, where as varieties with smaller lenticels of fruits are resistant to infection. Lenticels, that suberize rapidly are able to prevent the entry of the pathogen, as known in the case of potato scab pathogen Streptomyces scabies.

Internal structural barriers:

Similarly, the size and internal structure of lenticels has a direct bearing on the host resistance. Apple varieties having large lenticels on the fruit surface are easily accessable by Pseudomonas populosum,  the apple spot diseses bacterium, where as varieties with smaller lenticels of fruits are resistant to infection. Lenticels, that suberize rapidly are able to prevent the entry of the pathogen, as known in the case of potato scab pathogen streptomyces scabies. Several internal structure like thick and tough inner epidermal cell walls, extended sclerenchymatous hypodermis as found in the stems of many cerel crops, together with xylem, bundle sheath, and sclerenchyma cells of leaf veins are known to effectively block the spread of phytopathogens.

Post-infectional structural defence

The defence structure developed after successful penetration by pathogen within the host. Such development are in response to chain of reactions taking place between the host and the pathogen. Defence structures so developed include histological defence structures, cellular defence structure, cytoplasmic defence structure and necrotoic or hypersensitive defence reaction. These active, dynamic, post-infectional mechanism are considered to be of greater significance than pre-infectional ones in protecting plants against pathogens.

Historical defence structures
Post-infectional important histological barriers developed by reactive host include.

• Cork Layer Formation
• Abscission layer formation
• Tyloses formation
• Deposition of Gum

Cork layer formation

Various pathogens like fungi, bacteria, viruses, nematodes etc., are known to frequently induce formation of cork layers beyond the point of infection, as a result of stimulation of host cells by the substances secreted by the pathogen. Cork layers characteristics are:

• Impenetrable by pathogen due to thickness and strength of subrized cell walls of cork
• Blocks the spread of toxic substances secreted by the pathogen and prevents damage to underlying tissues.
• Stops the flow of nutrients and water from healthy to infected zone and thus ensures isolation of the pathogen by depriving from nutrational source.