Ultrastructural studies of the infection of susceptible and resistant cultivars of Sorghum bicolor by Colletotrichum sublineolum were conducted. Initial penetration events were the same on both susceptible and resistant cultivars. Germ tubes originating from germinated conidia formed globose, melanized appressoria, that penetrated host epidermal cells directly. Appressoria did not produce appressorial cones, but each penetration pore was surrounded by an annular wall thickening. Inward deformation of the cuticle and localized changes in staining properties of the host cell wall around the infection peg suggests that penetration involves both mechanical force and enzymic dissolution. In compatible interactions, penetration was followed by formation of biotrophic globular infection vesicles in epidermal cells. Filamentous primary hyphae developed from the vesicles and went on to colonize many other host cells as an intracellular mycelium. Host cells initially survived penetration. The host plasma membrane invaginated around infection vesicles and primary hyphae and was appressed tightly to the fungal cell wall, with no detectable matrix layer at the interface. Necrotrophic secondary hyphae appeared after 66 h and ramified through host tissue both intercellularly and intracellularly, forming hypostromatic acervuli by 114 h. Production of secondary hyphae was accompanied by the appearance of electron-opaque material within infected cells. This was thought to represent the host phytoalexin response. In incompatible interactions, infection vesicles and primary hyphae were formed in epidermal cells by 42 h. However, they were encrusted with electron-opaque material and appeared dead. These observations are discussed in relation to the infection processes of other Colletotrichum spp. and the host phytoalexin response.

SUMMARYCytological and physiological studies were conducted on the infection process of Colletotrichum sublineolum P. Henn. Kabat et Bub. on susceptible and resistant cultivars of Sorghum hicolor (L.) Moench. Compatible interactions were characterized by an early biotrophic phase lasting c. 24 h, during which intracellular infection vesicles and prin-iary hyphae colonized epidermal cells. 7 hinner secondary hyphae were first observed branching out from primary hyphae after 66 h. These hyphae proliferated throughout the epidermis and into underlying mesophyll cells. Secondary hyphae were associated with host cell death and the onset of a necrotrophic phase. Pigmented cytoplasmic inclusions, thought to represent the host defence response, were also first observed at 66 h, although there was little apparent effect on subsequent fungal colonization of tissue. By 90 h, secondary hyphae had proliferated throughout the leaf sheath, with production of necrotic lesions and acervuli. In incompatible interactions, infection vesicles formed inside epidermal cells within 42 h of inoculation but there was no evidence for a biotrophic interaction as penetrated cells appeared dead and fungal developmer>t was restricted to single epidermal cells. Host defence responses were observed earlier than in compatible interactions: heavily pigmented (dark red) cytoplasmic inclusions were distributed throughout penetrated cells at 42 h. By 66 h, these cytoplasmic inclusions had disintegrated and dark red pigment had spread throughout the cell. Concurrent with the disintegration of the cytoplasmic inclusions was the disruption of the cytoplasm of both the host cell and the fungus. Further fungal development was restricted. These observations are discussed in relation to the importance of the initial biotrophic phase in the successful colonization of S. bicolor by C. sublineolum and the role of the host defence response in preventing colonization.

The infection and colonization process of Colletotrichum acutatum on ripe blueberry fruit from two cultivars with different susceptibility to anthracnose were examined using light and confocal laser scanning microscopy. Ripe fruit from susceptible cv. Jersey and resistant cv. Elliott were drop-inoculated with a conidial suspension of C. acutatum, and epidermal peels were evaluated at selected times after inoculation and incubation. Results from pre-penetration studies demonstrated that there were significant differences in the rate of formation of melanized appressoria between the two cultivars, with the rate of formation being faster in the susceptible one. In both cultivars, penetration by the pathogen occurred via appressoria 48 h post-inoculation (hpi). However, in the susceptible cv. Jersey, C. acutatum then adopted an intracellular hemibiotrophic-like infection strategy, whereas in the resistant cv. Elliott subcuticular intramural-like infection occurred. In cv. Jersey by 108 hpi, intracellular growth of the pathogen led to the formation of numerous acervuli, with orange conidial masses. By 120 hpi, the conidial masses had coalesced covering the entire inoculated area. In cv. Elliott, acervuli were not seen until 144 hpi and contained few conidia. These results demonstrate for the first time the ability of C. acutatum to adopt a different infection and colonization strategy depending on the susceptibility of the host tissue being colonized.

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