Defence Mechanisms of Host | Plant Pathology

In this article we will discuss about the defence mechanisms of host.

Interaction between host and pathogen is a complicated process during which dis-balance host metabolic processes and formation of defence chemicals — phenolic substances take place. With the help of defence chemicals the host tries to repel the attack of the pathogen.

These chemicals are not only active against the inducer orga­nism but are also against any other pathogenic organisms leading to delay in symptom appearance and even total protection. Besides this, whether a plant is resistant to the attack of a pathogen or susceptible, and the degree of these qualities, is determined by the genetic characters of the host plant.

The Defence mechanisms in the host plant may be considered broadly under two heads:

(i) Resistance to host penetration and

(ii) Resistance to host invasion leading to disease development.

The former applies to all structures which oppose penetration and the latter to the host protoplasm conditions which decide the fate of the pathogen.

i. Resistance to Host Penetration:

The external and internal barriers present may be differentiated into:

Existing defence structures, some of them are—waxes and cuticle, thick and tough cell wall, dignified or silicified cell wall, and shape and size of stomata and lenticels; and post-infection defence structures, these may be —histological defence (formation of cork layers, development of abscission layers, formation of tyloses and deposition of gums), cellular defence structures (callus-like swellings of the cell wall and en-sheathing of penetrating hyphae), cytoplasmic defence reaction, necrotic or hypersensitive reactions.

In some resistant host plants infection stimulates the development of Calcium oxalate crystals which protect them against disease incidence. There may be antagonistic effect during host infection in which pectic enzymes are inactivated by toxins. High sugar content in the host tissue often suppresses production of pectic enzymes by pathogens.

Also high Calcium content confers disease resistance, possibly due to enhanced resistance to attack by certain polygalacturonases resulting from increased formation of Calcium pectate.

ii. Resistance to Host Invasion:

This may be designated as post-infection bio­chemical defence reaction (dynamic defence) or physiological or biochemical defence mechanism. As the pathogen grows rapidly accumulation of phenolic substances takes place in the host tissue particularly in case of incompatible host-pathogen com­bination than in compatible combination.

Higher plants contain large number and variety of aromatic substances which are precursors for the synthesis of phenolic sub­stances.

These phenolic substances pre-existing in the host plant tissue whose synthesis is accelerated by host infection are called common phenolics, whereas those which do not exist in the host tissue but are formed as a result of host-pathogen interaction are known as phytoalexins (alexin means to ward off).

Muller and Borger first in­troduced in 1940 the phytoalexin concept in plant pathology. Muller (1956) defined phytoalexins as “antibiotics, which are produced as a result of the interaction of two different metabolic systems—the host and parasite, and which inhibit the growth of the microorganisms pathogenic to plants.”

Hence phytoalexins are phenolic substances produced in the host tissue due to pathogen infection have antimicrobial properties.

The synthesis of phytoalexins is common in the hypersensitive reactions of pathogens and is more rapid in resistant than in susceptible host plants. Phytoalexins are nonspecific in their toxicity towards fungal pathogens although the latter may be differentially sensitive to the former.

The defense reaction is confined to the living- host tissue colonized by the pathogen and the speed with which phytoalexins are pro­duced depends upon the degree of resistance of the host.

It is determined by the concentration of phytoalexins. The sensitivity or capacity of the host to produce phyto­alexins is governed by genetic factors and a get e-for-gene relationship in host-pathogen reactions appears to be present.

Some examples of phytoalexins are:

Pisatin in Pisum sativum following infection by Ascochyta pisi, ipomeamatone in Ipomoea batatas following infection by Thielavia basicola. These substances may also be produced in other host plants in response to infection by other fungal pathogens.

Besides phytoalexins, phenols like chlorogenic acid, catechol, rufianic acid and cytokinins (kinetin, benzyladenine) act in defence reactions. Phenolic com­pounds may play an important role as natural inhibitors of pectolytic and cellulolytic enzymes. In general, increased phenol level in the host tissue gives resistance qualities in the host.

Several amino acid analogues like ethionine and phenylserine may also suppress the formation of enzymes. Various sugars and their derivatives may similarly suppress enzyme synthesis.

Many plants contain substances which can inhibit attack of fungi, bacteria and viruses, and disease resistance has frequently been attributed to such substances. These substances are: furocoumarin, isopimpinellin, oxazolinones, chlorogenic acid, caffeic acid, catechol and phloridzin.

There are reports that some phenolic compounds are converted into more highly fungitoxic substances, Such as quinones, as a response to infection. There is some recent evidence that sterols may be involved in defence reaction. Tomatine, a steroid of solanaceous plants may protect tomato leaves against some pathogens.

Fungal pathogen produces IAA-oxidase to inactivate the host auxin development while the host in turn inhibits the IAA-oxidase through formation of polyphenols like chlorogenic acid and caffeic acid. The enzyme peroxidase provides resistance in resis­tant host.

Again dehydrogenases and amino acid-oxidases are also part of defence reaction against fungal pathogen. Supply of Calcium and potassium also increases disease resistance of host plants. Again as a result of defence reaction, fusaric acid is detoxified by the host plant to a nontoxic compound N-methyl fusaric acid amide.

Besides above defence mechanisms, host plant may offer resistance to pathogen attack through:

(i) Hypersensitive reaction and

(ii) Inherited genetic charac­ter.

In case of hypersensitive reaction usually a small part of the plant tissue quickly dies after infection (necrosis) resulting in minor local lesion around the infection court. Inactivation or localization of the pathogen takes place preventing its further spread in the host tissue exhibiting defence reaction. This may result in the death of the pathogen by virtue of isolating in dead tissue or by its inactivation.

Several aspects of hypersensitive reaction are:

(a) Only living microorganisms and viruses are capable of inducing this reaction,

(b) It will occur only in incompatible host-pathogen .com­bination,

(c) At the initial stage of infection the pathogen multiplies at the same rate in either susceptible or resistant host, and

(d) The reaction appears earlier in resistant plants than do the typical symptoms in the susceptible plants. Such a defence reaction is often considered as an indication of a disease resistant variety.

The ability of a host plant to resist pathogen attack is an inherited genetic charac­ter. There are two types of genes for resistance— major and minor genes. Host plants having major gene resistance are usually highly resistant to specific races of a pathogen, resistance being conditioned by a single dominant gene and is stable over a wide range of environmental conditions.

Resistance can also be governed by minor genes with lesser efficiency, but not stable under varying environmental conditions. Major gene resistance is also designated as single dominant gene resistance or monogenic resistance. While resistance governed by minor genes is known as polygenic resistance.

This is due to the fact that resistance is usually inherited as a dominant character and is governed by one, two or more genes and the resistance is thus monogenic, bigenic, oli­gogenic or polygenic.