Abstract
Plants evoke innate immunity against microbial challenges upon recognition of pathogen-associated molecular patterns (PAMPs), such as fungal cell wall chitin. Nevertheless, pathogens may circumvent the host PAMP-triggered immunity. We previously reported that the ascomycete Magnaporthe oryzae, a famine-causing rice pathogen, masks cell wall surfaces with α-1,3-glucan during invasion. Here, we show that the surface α-1,3-glucan is indispensable for the successful infection of the fungus by interfering with the plant's defense mechanisms. The α-1,3-glucan synthase gene MgAGS1 was not essential for infectious structure development but was required for infection in M. oryzae. Lack or degradation of surface α-1,3-glucan increased fungal susceptibility towards chitinase, suggesting the protective role of α-1,3-glucan against plants' antifungal enzymes during infection. Furthermore, rice plants secreting bacterial α-1,3-glucanase (AGL-rice) showed strong resistance not only to M. oryzae but also to the phylogenetically distant ascomycete Cochlioborus miyabeanus and the polyphagous basidiomycete Rhizoctonia solani; the histocytochemical analysis of the latter two revealed that α-1,3-glucan also concealed cell wall chitin in an infection-specific manner. Treatment with α-1,3-glucanase in vitro caused fragmentation of infectious hyphae in R. solani but not in M. oryzae or C. miyabeanus, indicating that α-1,3-glucan is also involved in maintaining infectious structures in some fungi. Importantly, rapid defense responses were evoked (a few hours after inoculation) in the AGL-rice inoculated with M. oryzae, C. miyabeanus and R. solani as well as in non-transgenic rice inoculated with the ags1 mutant. Taken together, our results suggest that α-1,3-glucan protected the fungal cell wall from degradative enzymes secreted by plants even from the pre-penetration stage and interfered with the release of PAMPs to delay innate immune defense responses. Because α-1,3-glucan is nondegradable in plants, it is reasonable that many fungal plant pathogens utilize α-1,3-glucan in the innate immune evasion mechanism and some in maintaining the structures.
Highlights
The fungal cell wall, the outermost layer of the cell, is a physically rigid structure responsible for protecting the cell from environmental stresses and maintaining cell morphology
Magnaporthe oryzae, Cochlioborus miyabeanus, and Rhizoctonia solani are the top three fungal pathogens that are responsible for devastating damage to the production of rice, a staple cereal for half of the world’s population
Our study suggests that fungal surface a-1,3-glucan interferes with host immunity in many fungal pathogens and that a-1,3-glucan is a potential target for controlling various fungal diseases in plants
Summary
The fungal cell wall, the outermost layer of the cell, is a physically rigid structure responsible for protecting the cell from environmental stresses and maintaining cell morphology. The structural core of the fungal cell wall is composed of branched b-1,3-glucan cross-linked to chitin. This core complex is generally fibrillar and embedded in alkali-soluble polysaccharides that vary according to fungal species, growth stages and environments [1,2]. In plant-fungus interactions, plants recognize fungus-specific molecules, such as cell wall polysaccharides, cell membrane sterols and secreted proteins, as pathogenassociated molecular patterns (PAMPs) via pattern recognition receptors (PRRs) that initiate immediate innate immune responses, including the production of antifungal enzymes, anti-microbial metabolites and reactive-oxygen species, against a broad range of fungal invaders [3,4,5,6,7]. Fungal pathogens are able to infect host plants; they are expected to acquire some mechanisms to escape the recognition of their cell wall PAMPs by the host PRRs
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