Structural Characterisation of the Interaction between Triticum aestivum and the Dothideomycete Pathogen Stagonospora nodorum

Abstract

The interaction between Stagonospora nodorum and a susceptible wheat cultivar was investigated using a range of microscopic techniques. Germination of pycnidiospores occurred approximately 3 h after making contact with the leaf surface and was followed by attempted penetration 8-12 h later. Penetration was observed through stomata and also directly through periclinal and anticlinal epidermal cell walls. Penetration down the anticlinal cell walls appeared to occur without a differentiated penetrating structure whilst structures identified as either lateral appressoria or hyphopodia were typically present when penetrating over a periclinal cell wall. Once inside the leaf, the fungus continued to grow for the next 4-5 days colonising all parts of the leaf except the vascular bundles. Only in the later phase of the infection was total host cell collapse apparent. Evidence of polyphenolic compounds was observed. The infection cycle was completed within 7 days as indicated by sporulation on the leaf surface. These results have allowed us to understand how the fungus physically interacts with the leaf and will help the overall understanding of the infection process.

A Signaling-Regulated, Short-Chain Dehydrogenase of Stagonospora nodorum Regulates Asexual Development

“…Sampling time points were 1, 3, 5, and 8 days postinfection, which coincided with host penetration, proliferation, onset, and late pycnidiation, respectively (61). Six of the genes identified from the proteomic analysis showed significantly differential expression during infection of detached wheat leaves by S. nodorum (Fig.…”

Dothideomycete–Plant Interactions Illuminated by Genome Sequencing and EST Analysis of the Wheat Pathogen Stagonospora nodorum

“…It is interesting to note that although a range of Neurospora species all contained a gene orthologous to the class 1 hydrophobin EAS gene from N. crassa, they were expressed significantly only in species that produced aerial conidia (Winefield et al, 2007). S. nodorum produces pycnidiospores in a gelatinous cirrhus adapted for rain dispersal (Solomon et al, 2006b). It may be that the absence of aerial mitosporulation negates the need for class 1 hydrophobins.…”

“…For the construction of the in planta cDNA library, wheat (Triticum aestivum) cv Amery was infected with S. nodorum SN15 as a whole plant spray and processed as a latent period assay (Solomon et al, 2006b). Necrotic tissue was excised from the leaves at 10, 11, and 12 DAI for RNA isolation.…”

“…It is the major cause of losses due to foliar pathogens in Western Australia and north central and northeastern North America (Solomon et al, 2006a), and until the 1970s, it was the major foliar necrotrophic pathogen in Europe (Bearchell et al, 2005). Infection begins when spores (ascospores or asexual pycnidiospores) land on leaf tissue (Bathgate and Loughman, 2001;Solomon et al, 2006b). The spores rapidly germinate to produce hyphae that invade the leaf, using hyphopodia to gain entry to epidermal cells or by growing directly through stomata (Solomon et al, 2006b).…”

“…Infection begins when spores (ascospores or asexual pycnidiospores) land on leaf tissue (Bathgate and Loughman, 2001;Solomon et al, 2006b). The spores rapidly germinate to produce hyphae that invade the leaf, using hyphopodia to gain entry to epidermal cells or by growing directly through stomata (Solomon et al, 2006b). The hyphae rapidly colonize the leaves and begin to produce pycnidia in 7 to 10 d. The infection has been divided into three metabolic phases (Solomon et al, 2003a).…”