Abstract

A common response by plants to fungal attack is deposition of callose, a (1,3)-β-glucan polymer, in the form of cell wall thickenings called papillae, at site of wall penetration. While it has been generally believed that the papillae provide a structural barrier to slow fungal penetration, this idea has been challenged in recent studies of Arabidopsis (Arabidopsis thaliana), where fungal resistance was found to be independent of callose deposition. To the contrary, we show that callose can strongly support penetration resistance when deposited in elevated amounts at early time points of infection. We generated transgenic Arabidopsis lines that express POWDERY MILDEW RESISTANT4 (PMR4), which encodes a stress-induced callose synthase, under the control of the constitutive 35S promoter. In these lines, we detected callose synthase activity that was four times higher than that in wild-type plants 6 h post inoculation with the virulent powdery mildew Golovinomyces cichoracearum. The callose synthase activity was correlated with enlarged callose deposits and the focal accumulation of green fluorescent protein-tagged PMR4 at sites of attempted fungal penetration. We observed similar results from infection studies with the nonadapted powdery mildew Blumeria graminis f. sp. hordei. Haustoria formation was prevented in resistant transgenic lines during both types of powdery mildew infection, and neither the salicylic acid-dependent nor jasmonate-dependent pathways were induced. We present a schematic model that highlights the differences in callose deposition between the resistant transgenic lines and the susceptible wild-type plants during compatible and incompatible interactions between Arabidopsis and powdery mildew.

Highlights

  • A common response by plants to fungal attack is deposition of callose, a (1,3)-b-glucan polymer, in the form of cell wall thickenings called papillae, at site of wall penetration

  • We anticipated an improved resistance to the avirulent powdery mildew Blumeria graminis f. sp. hordei (Bgh) in Arabidopsis lines showing increased pathogen-induced callose deposition

  • Whereas higher callose accumulation contributes to resistance against nectrophic fungal pathogens, such as Alternaria brassicicola and Plectosphaerella cucumerina (Ton and Mauch-Mani, 2004), recent results have suggested that callose deposition is irrelevant for plant resistance to adapted biotrophic powdery mildews (Consonni et al, 2010)

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Summary

Introduction

A common response by plants to fungal attack is deposition of callose, a (1,3)-b-glucan polymer, in the form of cell wall thickenings called papillae, at site of wall penetration. We generated transgenic Arabidopsis lines that express POWDERY MILDEW RESISTANT4 (PMR4), which encodes a stress-induced callose synthase, under the control of the constitutive 35S promoter. In these lines, we detected callose synthase activity that was four times higher than that in wild-type plants 6 h post inoculation with the virulent powdery mildew Golovinomyces cichoracearum. The proposed function of callose as a barrier to retard invading pathogens was further challenged by studies using Arabidopsis (Arabidopsis thaliana) mutants lacking the stress-induced callose synthase POWDERY MILDEW RESISTANT4 (PMR4; known as GLUCAN SYNTHASE-LIKE5). Even though the involvement of callose in plant defense has been investigated for well over a century, the specific function of callose in plant-pathogen interactions has not been elucidated

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