The following points highlight the two methods employed by plants to cope with biotic stresses. The methods are: 1. Hypersensitive Response and 2. Secondary Acquired Resistance.
Method # 1. Hypersensitive Response (HR):
On being attacked by insects or a pathogenic microorganism, typically a plant responds with:
(i) Formation of pathogenesis-related (PR) proteins,
(ii) Biosynthesis of phytoalexins,
(iii) Changes in composition and physical properties of cell walls and finally
(iv) Process of programmed cell death wherein the cells immediately surrounding the infection site die rapidly to deprive the pathogen of nutrient supply and thus checking its spread in host plant and leaving a necrotic lesion at the site of invasion. All these responses are collectively known as hypersensitive response or reaction (HR).
A brief account of these follows:
(i) Pathogenesis-Related (PR) Proteins:
These are products of defense-related genes that are activated by microbial infection and include hydrolytic enzymes such as:
(i) Proteinase inhibitors which inhibit activities of proteolytic enzymes secreted by the pathogen, and
(ii) Lytic enzymes such as glucanases, chitinases, and other hydrolases that attack and degrade the cell walls of the pathogen.
(ii) Biosynthesis of Phytoalexins:
The microbial infection also activates genes that encode enzymes for the synthesis of phytoalexins. Phytoalexins are a chemical diverse group of secondary metabolites (chiefly isoflavonoids and sesquiterpenes) with strong antimicrobial activity. The isoflavonoids medicarpin from alfalfa and glyceolin from soybean and sesquiterpenes such as rishitin from tomato and potato and capsidiol from tobacco and pepper are well known examples of phytoalexins.
(iii) Changes in Composition and Physical Properties of Host Cell Walls:
In response to pathogen invasion, lignin, callose, suberin and some hydroxy-proline rich glycoproteins are synthesized and accumulated in host cell walls to strengthen the latter and physically blocking the spread of the invading pathogen.
(iv) Programmed Cell Death (PCD):
The hypersensitive response culminates in rapid death of cells around the infection site depriving pathogen of the nutrient supply and limiting its spread in host plant and leaving necrotic lesions (small regions of dead tissues) at the site of invasion. The rest of the plant however, remains unaffected. Recent researches have shown that the hypersensitive response is preceded by accumulation of nitric oxide (NO) and active oxygen species (including the superoxide anion O2–, hydrogen peroxide H2O2 and hydroxyl radical OH).
The production of active oxygen species (known as the oxidative burst) and nitric oxide (a secondary messenger in many signalling pathways in animals and plants) appears to be prerequisite for activation of hypersensitive response. Induction of PCD is prevented in absence of any of these two signals.
It is believed that a plasma membrane located NADPH dependent oxidase reduces the O2 to produce superoxide anions. The latter in turn are converted into hydrogen peroxide and hydroxyl radicals. The active oxygen species especially the hydroxyl radicals may contribute to PCD as part of the hypersensitive response or these may act to kill the pathogen directly.
A transient increase in cytosolic Ca2+ concentration is required for the activity of the enzyme NO synthase which converts the amino acid arginine into nitric oxide.
Consequent to pathogen infection, both oxidative burst and NO production are activated by a transient change in plasma-membrane permeability resulting in influx of H+ and Ca2+ ions into the cell and efflux of K+ and CI– ions.
Mechanism of Recognition of the Potential Pathogen to Initiate Defence Response in Plants:
Not all plants are resistant to disease caused by pathogens. Researchers have shown that resistance of plants to microbial pathogens has an underlying genetic basis. The pathogens carry avr genes (virulence genes) while the host plants carry corresponding resistance genes called R genes. Disease occurs when the pathogen lacks avr genes or the host plant does not carry dominant R genes.
The avr genes are believed to encode enzymes for the production of specific substances called elicitors while R genes encode protein receptors that recognise and bind with these elicitors to initiate the hypersensitive response.
The elicitors (L., elicere, to entice) are substances originating from pathogens that include proteins, peptides, sterols, and polysaccharide fragments arising from cell walls of pathogen or outer membrane or a secretion process. Sometimes, polysaccharide fragments resulting from initial degradation of the host plant cell walls by pathogen may elicit a hypersensitive response.
The receptor proteins encoded by R genes are located on plasma-membrane and have a leucine- rich domain which is repeated inexactly many times in the amino-acid sequence. These domains may extend outer or inner to the plasma-membrane and bind with specific elicitors to recognise the pathogen. (R genes comprise one of the biggest gene families in plants).
Method # 2. Secondary Acquired Resistance (SAR):
The hypersensitive response described earlier is limited to near vicinity of the initial site of infection by pathogen. But, often the entire host plants develops increased resistance against pathogens over a period of time ranging from few hours to several days following initial infection at one site of the plant. This phenomenon wherein “a single encounter with the pathogen increases resistance to entire plant to future attacks by pathogens” is called as secondary acquired resistance (SAR) and is part of the plant’s immune response.
SAR appears to result from increased levels of some secondary metabolites and other defense compounds such as chitinases and other hydrolytic enzymes. However, the mechanism of SAR is not clearly understood. One component of the signalling pathway is likely to be salicylic acid (SA) that is a benzoic acid derivative and a secondary metabolite. It has been shown in variety of plants that the infection by pathogen results in increased levels of SA in the zone of infection that establishes SAR in distant regions of the plant (Fig. 23.5).
According to Van Bel and Gaupels (2004), the transmission of SAR signal from infection site to other parts of the plant is very rapid (3 cm/h) and possibly occurs through vascular tissue. Phloem is now considered to be the pathway of SAR signal.
Salicylic acid is not the mobile SAR signal. Maldonado et al (2002) have shown that in Arabidopsis, mutations in DIR1 gene (Defective in Induced Resistance 1 gene) inhibit SAR response. This gene is specifically expressed in phloem and encodes a lipid-transfer protein and it has been suggested that the long distance SAR signal might be a substance derived from a lipid.
Apart from phloem-mobile signals, the plant may develop SAR through air-borne signals. Salicylic acid may be converted into its methyl ester, methyl salicylate that is a moderately volatile substance. (Structures of Salicylic acid and methyl salicylate are given in Fig. 23.6). Methyl salicylate may function as volatile air-borne SAR-inducing signal that is transmitted to distant non-infected parts of the plant and even to non-infected neighbouring plants making them resistant to pathogens attack.
