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Histopathology of Seed-Borne Infections - Applied Research Center ...

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Location <strong>of</strong> Fungal Hyphae in <strong>Seed</strong>s 115the common host, and the disease appears in the form <strong>of</strong> tumor-like swellings onaerial parts including flowers. The infection is partial and scattered on different parts.The infected fruits are hypertrophied, and they are called galls. The fungal myceliumand chlamyspores are found only in infected tissues (Gupta, 1962; Pavgi andMukhopadhyay, 1972; Rao, 1972; Singh, 1991).The healthy cremocarp is symmetrical and comprises two mericarps. The hypertrophiedand galled fruits are symmetrical or asymmetrical depending on whetherthe infection is complete or partial. The ridges on the surface <strong>of</strong> these fruits areinconspicuous, and the affected pericarp lacks differentiation. Its cells are uniformlyenlarged with prominent air spaces and abundant chlamydospores. The vittae arenot recognized and the vascular bundles are dispersed with poor thickening <strong>of</strong> xylemelements. The cells in the inner epidermis are tangentially stretched and thin-walled.The cells in carpophore are also hypertrophied, and its vittae and vascularbundles are inconspicuous. The pedicel and stylopodium, which remain with fruit,show hypertrophy <strong>of</strong> cells, prominent air spaces, distinct but reduced amount <strong>of</strong>vascular zone, indistinct vittae, and abundant mycelium and chlamydosphores. Inpartially infected fruits, the uninfected part shows normal anatomical features(Figure 5.7).The size <strong>of</strong> locules and the development <strong>of</strong> ovules are directly correlated withthe intensity <strong>of</strong> infection. In severely infected and fully hypertrophied fruits, theovules abort. In moderately hypertrophied fruits, the ovules develop to varyingextents and have endosperm and embryo, but the latter is weakly developed. Fruitswith chlamydospores confined only to the pericarp usually have well-formed seedswith a developed embryo. Such seeds germinate normally (Gupta, 1962).5.5.2.2 ClavicepsSpecies <strong>of</strong> Claviceps cause ergot disease in diverse graminaceous crops and grasses.The disease cycle (Figure 5.8) follows an almost uniform pattern. The path <strong>of</strong>infection and development <strong>of</strong> stroma and sclerotia under natural and experimentalconditions are known for Claviceps purpurea in rye (Tulsane, 1853; Campbell,1958), C. paspali in Paspalum dilatatum (Brown, 1916; Luttrell, 1977), C. fusiformisin pearl millet (Thakur, Rao, and Williams, 1984; Roy, 1984), and C. sorghi insorghum (Bandyopadhyay et al., 1990). The development <strong>of</strong> sclerotia follows twodifferent courses.Initial infection by ascospores (primary) and conidia (secondary) takes placethrough the stigma. The invading hyphae grow down the style (Figure 5.9A) andcolonize the ovary. In ovaries <strong>of</strong> rye infected by C. purpurea and pearl millet byC. fusiformis, the development begins at the base <strong>of</strong> ovary (Figure 5.9B, C) with theappearance <strong>of</strong> the sphacelial stage (Weihing, 1956; Roy, 1984). The affected tissues<strong>of</strong> the ovary produce sweet viscid fluid in which conidia remain embedded. It isexuded as honeydew. The apical part <strong>of</strong> the ovary resists disintegration, and it iscarried at the top <strong>of</strong> the sphacelial stroma. The downward colonization <strong>of</strong> the hostdoes not proceed beyond the plate <strong>of</strong> cells at the upper limit <strong>of</strong> rachilla (Figure 5.9C),where a tissue (plate) <strong>of</strong> four to six layers separates the infected ovary from the

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