|Curry, Kenneth - UNIV OF SOUTHERN MS|
|Abril, Maitza - UNIV OF SOUTHERN MS|
|Avant, Jana - UNIV OF SOUTHERN MS|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 23, 2002
Publication Date: October 1, 2002
Citation: Curry, K.J., Abril, M., Avant, J.B., Smith, B.J. 2002. Strawberry anthracnose: histopathology of Colletotrichum acutatum and C. fragariae. Phytopathology. 92:1055-1063 Interpretive Summary: Anthracnose diseases of strawberry are caused by the fungal pathogens Colletotrichum acutatum, C. fragariae, and C. gloeosporioides and may affect strawberry fruit, stolons, petioles, leaves, crowns, and roots. Anthracnose crown rot causes heavy losses due to plant death, while anthracnose fruit rot causes severe preharvest losses of developing fruit and significant postharvest losses of mature fruit. Little is known about the mechanism the fungal pathogens utilize to infect the strawberry host. This study investigated the initial infection of strawberry stolons and petioles by C. and C. fragariae to determine similarities and differences between them which should lead to the development of anthracnose resistant strawberry cultivars. It was determined that both species invade in a similar manner; the initial invasion is biotrophic (the host cells remain alive), then reverts to necrotrophic (host cells are killed) once inside the strawberry host where cortical cell walls are disrupted. However, epidermal and subepidermal cells remained intact. This study also used cytochemical labeling techniques at the ultrastructural level to determine that C. fragariae expressed little or no masking of the chitin in its cell walls once it was inside the plant tissue. The fungus grew rapidly through the host aploplst before invading host cells. Most host cells were dead upon fungal entrance. This information will be useful to other scientists studying anthracnose diseases and how to control them.
Technical Abstract: Anthracnose is a severe disease of strawberry and may be caused by several Colletotrichum spp. including C. fragariae and C. acutatum. Ontogeny of the invasion process by C. acutatum and C. fragariae was studied on petioles and stolons of the strawberry cultivar Chandler using light and electron microscopy. Following cuticular penetration via an appressorium, subsequent steps of invasion involved hyphal growth within the cuticle and within the cell walls of epidermal, subepidermal, and subtending cells. Both species of fungi began invasion with a brief biotrophic phase before entering an extended necrotrophic phase. Acervuli formed once the cortical tissue had been moderately disrupted and began with the development of a stroma just beneath the outer periclinal epidermal walls. Acervuli erupted through the cuticle and released conidia. Invasion of the vascular tissue typically occurred after acervulus maturation and remained minimal. Some plant pathogens mask or modify potential elicitors, such as fungal wall chitin, perhaps to avoid host defenses, such as chitinase. The distribution of chitin in fungal walls was identified with gold labeled wheat germ agglutinin, a lectin probe, applied to the strawberry which was inoculated with C. fragariae. Ultrastructural observations of the chitin probe indicate that the inner layer of bilayered walls of conidia, germ tubes, and appressoria contain more chitin than unilayered invasive hyphae. The distribution of chitin in fungal walls of early invasive hyphae was similar to the distribution in late invasive hyphae and in the walls of fungi grown outside the host. This new finding constitutes an important insight into the epidemiology of this pathogen.