Histology of Disease Development in Resistant and Susceptible Cultivars of Chickpea (Cicer arietinum L.) Inoculated with Spores of Ascochyta rabiei

Abstract

Histological studies were performed on a compatible and an incompatible interaction between chickpea (Cicer arietinum L.) plants and the fungus Ascochyta rabiei (Pass.) Labr. The time course of infection, development on leaflets and stems of susceptible (ILC 1929) and resistant (ILC 3279) plants was monitored by light or scanning electron microscopy with the aim to compare histological changes as the basis for further work on biochemical changes in this plant‐pathogen interaction. Spores of A. rabiei began to germinate from 12 hpi on and developed a polar germ tube; fungal colonization, secretion of a mucilaginous exudate and appressoria formation (1–3 dpi) were identical on both cultivars. Leaves of susceptible plants were invaded by the fungus directly through the cuticle, the fungus then spread subepidermally followed by a rapid collapse of the leaf tissue (4–6 dpi). Development of leaf spots and fungal pycnidia could be observed 6–8 dpi. The resistant cultivarrapidly responded (24–48 hpi) to fungal infection and cells of the palisade parenchyma exhibited autofluorescence. In later stages of the infection (4–5 dpi) fluorescent areas developed to small necrotic spots all over the leaflet. These necrotic areas, were the result of cell death and a subsequent change in the leaf structure and were characterized by the accumulation of phenolic compounds. Leaves of the resistant cultivar were invaded by the fungus to less than 5%.

Ascochyta blight of chickpea: infection and host resistance mechanisms

“…Ascochyta rabiei normally penetrates chickpea plants through the leaflet cuticle, following spore germination, germ tube elongation, and the formation of an appressorium-like infection structure (Höhl et al 1990; Ilarslan and Dolar 2002;Köhler et al 1995). Penetration occurs through the wall of epidermal cells, without invading the protoplast.…”

“…In resistant cultivars, plants show autofluorescence in the epidermal and palisade parenchyma cells, and the infected site turns brown immediately after the invasion by the pathogen. These autofluorescent spots later turn into necrotic spots (Höhl et al 1990;Ilarslan and Dolar 2002). As a result, growth of A. rabiei stops in the apoplastic space, whereas hyphae rapidly spread in the apoplastic space in susceptible cultivars.…”

“…In susceptible cultivars, plant cells lose their normal shape and the cellular structure disintegrates soon after subepidermal expansion of the hyphae (Höhl et al 1990). In resistant cultivars, plants show autofluorescence in the epidermal and palisade parenchyma cells, and the infected site turns brown immediately after the invasion by the pathogen.…”

“…However, in chickpea, several studies did not allow to correlate resistance to ascochyta blight with trichome density, acidity of exudate, or the activity of malate synthesis enzymes (Chand et al 1988;Singh and Chand 1997;Singh et al 1996). Histological studies have demonstrated that phases of fungal development outside the plant, e.g., spore germination, hyphal elongation, and appressorium formation, are essentially identical for both resistant and susceptible cultivars (Angelini et al 1993;Höhl et al 1990;Ilarslan and Dolar 2002). Dilution of exudate concentration by rainfall reduces the inhibitory effect of glandular exudates on spore germination and infection.…”

“…In addition to cutin, other major structural components of plant cell walls are pectin and xylan. Germ tubes of A. rabiei secrete large amounts of a mucilaginous exudate that produce a tight contact to the cuticle (Höhl et al 1990). This exudate also seals the infection site and protects germ tubes from desiccation.…”