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All plants possess active defence mechanisms against pathogen attack. But when the plant is infected by a virulent pathogen these mechanisms fail, because the pathogen avoids the effects of activated defences. If defence mechanisms are triggered by a stimulus prior to infection by a plant pathogen, disease can be reduced. Induced resistance is a state of enhanced defensive capacity developed by a plant when appropriately stimulated (Van Loon, Bakker, & Pieterse, 1998).
It is well established fact that certain types of infection or other treatments can induce disease resistance (Rocha & Hammerschmidt, 2005). The induced plant produce resistance to pathogens attack due to the enhanced ability to rapidly express defence upon infection and in some cases, an increase in defence that were resulted in response to the induced treatment. There are two basic assumptions to explain the phenomenon of induced resistance. First of all, plant must have all genes necessary to express an efficient defence. Second, the inducing treatment must be capable of activating some of the defences directly (Ray Hammerschmidt, 2007). The phenomenon of induced resistance results in reduction in lesions incidence and severity but is unable to completely control the pathogens (Ku 1982). Induced resistance to microbial pathogen can be split broadly into systemic acquired resistance (SAR) and induced systemic resistance (ISR).
Systemic acquired resistance (SAR) and induced systemic resistance (ISR)
Systemic acquired resistance (SAR) refers to the development of a broad-spectrum systemic resistance to pathogenic attack after a localized infection either as a part of the hyper-sensitive response (HR) or subsequent to recent treatment, the SAR pathway is activated (Walters, Walsh, Newton, & Lyon, 2005). The development of SAR is associated with the elevated levels of salicylic acid (SA) locally and systemically with the coordination of expression of a specific set of genes encoding pathogenesis-related (PR) protein (Van Loon, Rep, & Pieterse, 2006).
During SAR, resistance reactions taking place in the non-infected parts of the pre-treated plants can be studied separately from reactions occurring at the infection site (Metraux, Nawrath, & Genoud, 2002). At the site of attack, the resistance responses of the host include modifications of the cell wall, production of phytoalexins (R Hammerschmidt, 1999a), synthesis of pathogenesis related (PR) proteins (Van Loon & Van Strien, 1999). At the systemic level, the production of PRs before a challenge infection is the most commonly observed reaction. In contrast, other reactions such as changes in cell wall lignifications were detected after challenge infection of the upper leaf but with faster induction kinetics (Sticher, Mauch-Mani, & Métraux, 1997).
Unlike SAR, induced systemic resistance (ISR) is not associated with local necrotic lesion formation. ISR also differs in that it depends on perception of ethylene and jasmonic acid rather than association with expression of salicylic acid (SA) and PR genes. ISR is induced by certain strains of plant growth promoting rhizobacteria (PGPR) (Ray Hammerschmidt, 2007). Various natural and synthetic substances activate SAR or ISR in horticultural produce. True chemical activators modify the plant pathogen interaction, so that it resembles an incompatible interaction with defence related mechanisms induced prior to or after challenge (Sticher, et al., 1997).
Salicylic acid (SA), ethylene (ET), and jasmonic acid (JA) are the main signaling molecules involved in defense responses (Chen, Zhang, & Yu, 2010). The SA signaling pathway is mainly linked to resistance to biotrophic pathogens. The JA and ET signaling pathways mediate resistance mainly to necrotrophic pathogens. Thus, there are complicated defense networks that are induced in response to different types of invading pathogens. Interestingly, the SA and ET/JA signaling pathways often interact in an antagonistic manner (Kunkel and Brooks 2002).
Salicylic acid (SA)
Salicylic acid (SA) is a well known natural inducer of disease resistance in plants (Sticher, et al., 1997). Pre-harvest and/or postharvest applications of 2.0 mg SA mlâˆ’1 tended to restrain postharvest anthracnose disease severity caused by Colletotrichum gloeosporioides in mango fruit (Zainuri, Wearing, Coates, & Terry, 2001). However, it was not clear whether SAR was induced. Zainuri et al. (2001) attributed the effects of SA to inhibition of mango skin ripening. Ripening retardation was probably through an anti-ethylene affect as seen in banana (Srivastava & Dwivedi, 2000) and not due to enhancement of endogenous antifungal activity in the skin of mango fruit. An ethylene-suppression role may extend the shelf life of the fruit, thus delaying the expansion of disease symptoms that normally develop as climacteric fruit ripen (Zainuri, et al., 2001). However, SA (0.1-2.0 mg mlâˆ’1) when applied as a postharvest dip, was ineffective in suppressing grey mould caused by Botrytis cinerea after harvest on strawberry and Camarosa fruit, respectively. In contrast, natural defence resistance (NDR) against B. cinerea was enhanced in kiwifruit dipped in SA (0.14 mg mlâˆ’1) before storage (Poole and McLeod, 1994; Poole et al., 1998). SA treatment resulted in increased phenylalanine ammonia-lyase (PAL) and peroxidase activities relative to untreated control fruit (P. R. Poole, et al., 1998). Contradictory results between fruit types may highlight a difference in efficacy of SA treatment to elicit an induced response and/or interaction with ethylene for both climacteric and non-climacteric fruit (Terry & Joyce, 2004).
The signal for SAR
SA has been proposed to be the signal for induced resistance. This is based on the protective action of SA and various experimental evidences, including the over expression of a bacterial salicylate hydroxylase in transgenic plants that effectively reduces the level of endogenous SA (Sticher, et al., 1997). Grafting experiments in tobacco as well as leaf removal experiments in cucumber support the idea that SA is not the primary mobile signal exported from the infected leaf to other parts of the plant (Rasmussen, Hammerschmidt, & Zook, 1991). However, transport experiments in tobacco and cucumber have shown that SA moves from its production site in the infected leaf to the upper leaves by the phloem (Molders, Buchala, & Metraux, 1996).
Jasmonic Acid (JA)
Jasmonic acid (JA) and its methyl ester, methyl jasmonate (MeJA), have been found to occur naturally in a wide range of higher plants. It is a final product of the enzymatic oxidation of unsaturated fatty acids and lipoxygenase (LOX) (Vick & Zimmerman, 1984). Jasmonate has been shown to increase the chilling tolerance of several plant species (Wang & Buta, 1994). In addition, postharvest decay of strawberries caused by Botrytis cinerea was reduced by exposure of the fruit to MeJA vapour (Moline, Buta, Saftner, & Maas, 1997). After MeJA treatment, the storage life of fresh-cut celery sticks and bell-pepper slices was extended by reduction of microbial growth and decreased physiological deterioration (Buta & Moline, 1998). However, the mechanism of MeJA treatment used to protect against decay and chilling injury is unclear (Ding, Wang, Gross, & Smith, 2002). In the past decade, research on the defense signaling pathways that are activated by beneficial microorganisms revealed that JA and ET are central players in the regulation of ISR.
Jasmonic acid (JA), a fatty-acid-derived signaling molecule, is involved in several aspects of plant biology including pollen and seed development, and defense against wounding, ozone, insect pests and microbial pathogens (Creelman & Mullet, 1997; Li, Li, & Howe, 2001; Reymond & Farmer, 1998). The pathogens employ a common virulence strategy that involves rapidly killing plant cells to obtain nutrients, and thus are often referred to as 'necrotrophs' (Jackson & Taylor, 1996). Several JA-dependent genes that encode pathogenesis-related proteins, including plant defensin1.2 (pdf1.2) thionin2.1 (thi2.1), hevein-like protein (hel) and chitinaseb (chib), are commonly used to monitor JA-dependent defense responses (Reymond & Farmer, 1998).
Several mutants that exhibit enhanced or constitutive JA responses have been isolated (Ellis & Turner, 2001). It seems likely that constitutive JA-signaling mutants would exhibit enhanced resistance to necrotrophic pathogens that are normally controlled by the JA pathway. Consistent with this hypothesis, A. thaliana plants that overexpress a JA-biosynthetic gene constitutively express PDF1.2 and exhibit enhanced resistance to B. cinerea (Seo, et al., 2001).
The role of Ethylene (ET) in plant defense is somewhat controversial as it contributes to resistance in some interactions (Norman-Setterblad, Vidal, & Palva, 2000), but promotes disease production in others (Bent, Innes, Ecker, & Staskawicz, 1992). For example, the ethylene insensitive2 (ein2) mutant of A. Thaliana exhibits increased susceptibility to B. cinerea (Thomma, Eggermont, Tierens, & Broekaert, 1999) and E. Carotovora (Norman-Setterblad, et al., 2000), but decreased symptoms when infected with virulent isolates of P. syringae or Xanthomonas campestris (Bent, et al., 1992). The JA and ET signaling pathways are also both required for the induction of induced systemic resistance (ISR), a form of systemic resistance that is triggered by the root-colonizing bacterium P. fluorescens (Pieterse & van Loon, 1999) . These observations have lead to the development of simple models in which ET and JA are placed together in a single signaling pathway (Fig.1). However, these models are likely to be too simple, as the JA and ET signaling pathways have also been shown to modulate each other (Kunkel & Brooks, 2002).
Figure. 1. A working model of the SA, JA and ET pathogen defense pathways in Arabidopsis thaliana (Kunkel & Brooks, 2002).
The Hypersensitive Response (HR)
The term hypersensitive response (HR) refers to the localized and rapid death of one or a few host plant cells in response to invasion by an avirulent pathogen (Goodman & Novacky, 1994). HR is characterized by a rapid loss of membrane integrity in the infected host cells and the accumulation of brown phenolic compound oxidation products (Goodman and Novacky, 1994). Although HR may be an effective defence against oblige parasites that require living host cells for nutrition, it is likely that this response is only a single part of the defensive strategy of the plant because some host responses do not result in the HR (R Hammerschmidt, Bonnen, Bergstrom, & Baker, 1985).
Pathogenesis related protein (PR)
The hypersensitive reaction to a pathogen is one of the most well-organized defence mechanisms in nature and leads to the initiation of numerous plant genes encoding defence proteins. Pathogenesis-related (PR) proteins represent major quantitative changes in soluble protein during the defence response. The PRs have typical physicochemical properties that enable them to resist to acidic pH and thus survive in the harsh environments. Since the discovery of the first PRs in tobacco many other similar proteins have been isolated from tobacco but also from other plant species, including dicots and monocots, most of them from hypersensitively reacting tobacco (Stintzi, et al., 1993). Most PR proteins are induced through the action of the signaling compounds salicylic acid, jasmonic acid or ethylene (Van Loon, et al., 2006)
PR proteins remained absent in healthy plants but accumulating in large amounts after infection (Van Loon & Van Kammen, 1970), they have now been detected in more than 40 species (van Loon, 1999). Two groups of PR proteins can be distinguished. Acidic PR proteins are predominantly located in the intercellular spaces. Basic PR proteins are functionally similar but have different molecular weights and amino acid sequences and are mainly located intracellularly in the vacuole (van Loon, 1999). Some PR proteins have chitinase (Legrand, Kauffmann, Geoffroy, & Fritig, 1987) or b-1,3-glucanase activity. Chitinases are a functionally and structurally diverse group of enzymes that can hydrolyse chitin, and several are believed to contribute to the defence of plants against certain fungal pathogens (Jackson & Taylor, 1996). In contrast, the function of other PR proteins is still unknown (Van Loon & Van Strien, 1999) and many of them may be functionally active only when combined. Some PR proteins, most prominently the basic ones, are also expressed constitutively in a tissue-specific and developmentally controlled manner (Van Loon & Van Strien, 1999). It has been indicated that at least some inducible defense-related proteins are produced under specific physiological conditions (Van Loon, et al., 2006). Abiotic stresses such as to osmotic stress, cold stress or wounding can also result in defense-related protein initiation (Broekaert, Terras, & Cammue, 2000).
Phytoalexin and phytoanticipin
Plant responses to the infection with the synthesis of low molecular weight antibiotics known as phytoalexin (Kuc, 1995). The original concept of phytoalexins was of compounds that were specifically involved in host resistance. However, phytoalexin are now generally defined more broadly as compounds that are antimicrobial and induced after infection (VanEtten, Mansfield, Bailey, & Farmer, 1994). Phytoalexin accumulation is not limited to infection, although it occurs after infection. As phytoalexin research progressed, many modified definitions for phytoalexins have been proposed. It can be termed as "phytoalexins are low molecular weight antimicrobial compounds produced by plants in response to infection or stress" (Kuc, 1995). The accumulation of phytoalexins after infection may just reflect in response to stress caused by infection. Phytoalexin synthesis and accumulation does not require specific structural components of fungi, bacteria and viruses, or microbial metabolites as elicitors. The three groups of pathogens, as well as nematodes, have been reported to elicit accumulation of the same phytoalexins in some plants (Kuc, 1995). Over 200 compounds, microorganisms, and physiological stresses have been reported to elicit pisatin accumulation in pea, phaseollin and kievitone accumulation in green bean, and the glyceollins in soybean (Kuc, 1991). Plant constituents released after injury or infection can also function as elicitors (Dixon, 1986; Dixon, Harrison, & Lamb, 1994). Some fungicides, low temperature, and ultraviolet radiation also elicit accumulation of phytoalexins (Hadwiger & Schwochau, 1971; Mercier, Arul, & Julien, 1993). Consequently, the determinant for phytoalexin synthesis and accumulation is likely to be metabolic stress and not the structures of elicitors except as they cause metabolic stress (Kuc, 1995).
Distinguishing plant antibiotics is based on fundamental differences in the responses of plants to plant associated microorganisms. For a phytoalexin to serve as the basis of a disease resistance mechanism, there must be an active response on the plant's part, in which communication between plant and microorganism redirects the plant's metabolic activity. However, for a phytoanticipin to serve as the basis of a resistance mechanism, the plant relies on preformed compounds and can be passive in its relations with a potential pathogen (VanEtten, et al., 1994).
Cell wall modification
Cell wall is the first barrier which most pathogens encounter (Schafer, 1994), most of pathogens pass through it without apparent difficulty. However, plants cells may respond quickly to the pathogen attack by modifying cell wall in more effective manner, possibly act as diffusion barrier that block the flow of nutrients to the pathogens or toxin to the host cell (Ride, 1978). Lignification and deposition of phenolic compound is one type of cell wall modification that has been correlated with resistance (R Hammerschmidt & Nicholson, 2000). Nafussi et al. (2001) observed that hot water dip of lemon fruit inoculated with Penicillium digitatum triggers the production of lignin in the inoculated sites, which inhibits the growth of pathogen. The host cell often deposit lignin or some type of phenolic material in its cell wall at the point of fungal attack during the early stages of infection (R Hammerschmidt, et al., 1985). These deposits of lignin result in the blockade of fungal progression (Stein, Klomparens, & Hammerschmidt, 1993). If the cell wall lignifies after the penetration of infection, the entire cell may lignify resulting in the potential trapping of the pathogen in lignified chamber (R Hammerschmidt, et al., 1985). In addition to lignin, Î²- 1,3-glucan callose (Aist, 1983), hydroxyproline-rich glycoproteins (R. Hammerschmidt, Lamport, & Muldoon, 1982) and silicon oxides (Stein et al 1993) have also been reported to accumulate in the host cell walls as response to infection (R Hammerschmidt & Nicholson, 2000).
It is believed that the detection of pathogens is mediated by chemical substances secreted by the pathogens. Various types of such compounds (elicitor molecules) including oligosaccharides and lipids, have been revealed to induce defence responses in plant cells and they detect the potential pathogens in plant (Farmer, Moloshok, Saxton, & Ryan, 1991). Oligosaccharides derived from fungal and plant cell wall polysaccharides are one class of well characterized elicitors that, in some cases, can induce defence responses at a very low concentration. In view of their well-defined chemical nature and the presence of highly sensitive perception systems in plants, some of these elicitors have provided good model systems to study how plant cells recognize such chemical signals and transduce them for activation of the defence machinery (Shibuya & Minami, 2001).
Heat shock protein (HSP)
Changes in environmental conditions such as temperature, light, water status and hormone balance lead to altered gene expression in plants. At the molecular level, one of the best environmental responses is the response to high temperature or heat shock (Vierling, 1991). It has been shown that when seedlings are shifted to temperatures five or more degrees above optimal growing temperatures, synthesis of most normal proteins and mRNAs is repressed, resulting in transcription and translation of "heat shock proteins" (HSPs) (Key, et al., 1985). Plants develop tolerance to normally lethal temperatures if they are first subjected to certain treatments at high but nonlethal temperatures. In plants, as well as in other organisms, considerable evidence suggests that HSP production is an essential component of this short-term development of thermotolerance (Kimpel & Key, 1985a). Heat is not the only stress treatment that leads to high expression of many HSPs. Ethanol, arsenite, heavy metals, amino acid analogues and a number of other treatments affect the production of some HSPs in different organisms (E. Czarnecka, Nagao, Key, & Gurley, 1988). Although HSP have also been referred to as stress protein (Nagao, Kimpel, Vierling, & Key, 1986), but in plants, most HSPs are not synthesized in response to water stress (unless accompanied by heat stress) (Kimpel & Key, 1985b), anaerobic stress (Russell & Sachs, 1989), cold stress (Guy, 1990), or salt stress (E Czarnecka, Edelman, Schöffl, & Key, 1984). It is evident that production of HSPs occurs in response to specific changes not common to all stresses (Vierling, 1991).
Pressure shock and induced resistance
Plant produces induced resistance as a result of physiological stress (R Hammerschmidt, 1999b), in other words this response might be due to stress caused by infection (Kuc, 1995). Lurie (1998) also mentioned that slight stress condition can induce resistance in plants. Romanazzi et al (2001) reported that stress produced due to short hypobaric pressure treatment of sweet cherries and table grapes resulted in reduction of fungal decay. Similarly the short hyperbaric treatment of sweet cherries and table grapes controlled the postharvest fungal decay (Romanazzi, Nigro, & Ippolito, 2008), these treatments might have induced stress, resulting in the increased production of phytoalexins (R Hammerschmidt, 1999b). From the above discussion it is evident that postharvest stress produced due to pressure change in horticultural commodities might create higher induced resistance resulting in decay reduction.