Mechanisms of Resistance to Colletotrichum Species
Plants have a wide array of physical and chemical strategies to defend themselves from invasion by pathogens. Host resistance can be based upon physical factors such as surface features (e.g. topography, leaf hairs, and epicuticular waxes), that impede the formation of infection structures; structural barriers such as papillae that impede penetration; and secondary metabolites that are toxic or otherwise inhibitory to fungal growth (Heath, 1981). Physical barriers such as the mechanical strength of the cuticle and epidermal wall and the resistance of their structural polymers to enzymatic degradation, represent the first line of defense to fungal pathogens and may contribute to the greater resistance to several species of Colletotrichum of mature leaves and stems compared to young plant organs (Mercer et al., 1975). However, the active biochemical defence strategies adopted by plants to ward off fungal attack are generally considered to be more important as these often determine the success of an infection.

A common feature of a host resistance reaction expressed in response to infection is the rapid localised death and browning of host cells, known as a hypersensitive reaction (HR) (Bailey, 1982). O’Connell and Bailey (1986) distinguished two kinds of resistance using the bean anthracnose pathosystem (C. lindemuthianum-P. vulgaris). These were a form of resistance involving the early death of epidermal cells, and a form associated with delayed death of infected cells. In many resistant cultivars, single epidermal cells died as soon as they were in contact with the pathogen. This type of resistance, which seems to depend on the localised accumulation of phytoalexins (low molecular weight secondary metabolites with antimicrobial activity, formed de novo in response to infection), has been referred to as an example of HR based on host cell incompatibility (Bailey, 1983). Where resistance was associated with the delayed death of infected cells, initial events resembled those of susceptible interactions. However, after a biotrophic phase of varying duration, the infected cells died rapidly, turned brown and further fungal growth was prohibited (Elliston et al., 1976; Mercer et al., 1974). The extent of symptom and pathogen development appears to depend on the time at which the infected cells die, turn brown and accumulate phytoalexins (O’Connell and Bailey, 1986). However, a critical investigation of the HR by Bailey et al. (1980) indicated that early death of infected cells occurred before phytoalexin formation.

Not all plants respond to infection by Colletotrichum species by synthesising phytoalexins. For example no phytoalexins were detected in melon or cucumber infected with C. lagenarium. However, in this case the lignin content of melon cell walls increased upon infection, and it has been suggested that this is an alternative resistance mechanism (Grand and Rossignol, 1982).

Hydroxyproline-rich glycoproteins (HRGPs) are another group of metabolites often associated with host resistance. These compounds are usually present in low concentrations in the cell walls of higher plants, but in some interactions, e.g. C. lagenarium-melon they accumulate to high levels (Esquerré-Tugayé, 1973; Esquerré-Tugayé and Mazau, 1974). It has since been reported that HRGPs accumulate in bean and alfalfa seedlings infected with Colletotrichum species, and that greater amounts are produced in resistant tissues than in susceptible ones ( Mazau and Esquerré-Tugayé, 1986). HRGPs have also been shown to accumulate in papillae of Phaseolus vulgaris, produced in response to infection by C. lindemuthianum (O’Connell et al., 1991). The precise role of HRGPs in plant defense is unknown, but it has been suggested that they act by increasing the structural resistance of cell walls to pathogen penetration. In addition to HRGPs, other plant defense proteins are thought to be secreted at the host-pathogen interface (Esquerré-Tugayé et al., 1992). These include protein inhibitors of fungal hydrolases, and plant hydrolases (b -1,3-glucanases and chitinases) which exert their hydrolytic activity towards bacterial and fungal cell walls, causing lysis and/or release of elicitor-active fragments (Esquerré-Tugayé et al., 1992).

Formation of wall appositions (papillae) is often observed in the living cells of both resistant and susceptible hosts. These papillae are largely composed of callose, together with HRGPs and phenolics, and are deposited between the plasma membrane and outer wall of epidermal cells at sites of attempted fungal penetration (Bushnell and Gay, 1978; Skipp and Deverall, 1972; O’Connell et al., 1985). It has been suggested that the production of papillae may be stimulated by events which take place before the cuticle has been fully penetrated, such as the diffusion of fungal metabolites or by-products of cuticle degradation (Politis, 1976; Mould et al., 1991; O’Connell and Bailey, 1986). Although a proportion of intracellular hyphae can become completely encased by wall appositions and fail to develop further, papillae do not prevent all infections. It is probable that papilla deposition occurs in all penetrations, but in successful infections the response is ‘switched off’ and the fungus grows through the papilla. This would account for the callose ‘collar’ formed around the neck of haustoria and infection vesicles. In legumes, the proportion of hyphae encased by papillae that fail to develop further is low (5 - 15 %), but in grasses and cereals the proportion can be much greater (70 - 100%) (Politis, 1976; Sherwood and Vance, 1980).

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Mechanisms of Resistance in Sorghum
Juvenile sorghum plants rarely exhibit visible symptoms of infection when challenged with fungal pathogens such as C. sublineolum (Nicholson, 1988). This apparent expression of resistance has been attributed to the presence of substantial levels of the preformed cyanogenic glycoside, dhurrin, in juvenile sorghum leaves (Ferreira and Warren, 1982). However, studies have shown that fungal pathogens, including C. sublineolum, can detoxify hydrogen cyanide, which is the toxic breakdown product of dhurrin (Fry and Munch, 1975; Fry and Evans, 1977; Myers and Fry, 1978). It has therefore been suggested that dhurrin probably acts more as an insect feeding deterrent than as an antimicrobial compound involved in disease resistance (Woodhead et al., 1980; Nicollier et al., 1983).

It has been shown that young sorghum leaves accumulate a complex of phenols in response to invasion by both pathogenic and non-pathogenic fungi, and the five major components of this complex are the 3-deoxyanthocyanidin flavonoids (Figure 1): apigeninidin, luteolinidin, arabinosyl-5-O-apigeninidin, 7-methylapigeninidin, and 5-methoxyluteolinidin (Nicholson et al., 1988; Hipskind et al., 1990; Lo et al., 1996). All five of these compounds have exhibited fungitoxic activity towards C. sublineolum, and are considered to be phytoalexins (Nicholson et al., 1988). In leaf tissue, these phenolics first appear in the cell being invaded, accumulating in inclusions in the cytoplasm (Snyder & Nicholson, 1990; Snyder et al., 1991). These cytoplasmic inclusions migrate to the site of penetration, become pigmented, lose their spherical shape and ultimately release their contents into the cytoplasm, killing the cell and restricting further pathogen development.

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