Abstract

Ascochyta rabiei (teleomorph Didymella rabiei) is a directly penetrating, necrotrophic fungus that infects all aboveground parts of chickpea (Cicer arietinum). During spore germination and infection, germ tubes secrete a mucilaginous substance to facilitate attachment to the host surface, and the invading fungus produces cell-wall-lytic enzymes to penetrate the host. The pathogen produces several phytotoxins (solanapyrones A, B, and C, cytochalasin D, and a proteinaceous toxin) that seem to be responsible for necrosis and cell death. The pathogen can degrade antimicrobial compounds and suppress their production in chickpea. On the basis of aggressiveness, the population of A. rabiei can be classified into two broad pathotypes: pathotype I (less aggressive) and pathotype II (aggressive). Complete resistance to A. rabiei has not been found in chickpea; the resistance present in superior cultivars used in chickpea production is partial or incomplete. There is a high degree of variation in resistance among chickpea cultivars, and the resistance declines as the plant matures. The symptoms of infection and disease severity follow a quantitative continuum based on aggressiveness of the pathogen, genetic resistance present in the cultivar, and age of the plant. The well-established defense responses in chickpea are cross-linking of cell walls mediated by hydrogen peroxide, production of pathogenesis-related (PR) proteins (chitinase, β-1,3-glucanase, and thaumatin-like proteins), and accumulation of phytoalexins. However, expression of these induced defense responses does not correlate with pathotype-specific resistance, indicating that other constitutive or unknown components may be involved in providing resistance to aggressive pathotypes. Lack of information about the attribute that makes the pathogen aggressive, as well as inadequate knowledge of pathotype-specific defense mechanisms and the causes for decline in resistance, are major constraints in developing cultivars with durable resistance.

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