Cytology and physiology of infection of Phaseolus vulgaris by Colletotrichum lindemuthianum

Abstract

The progress of infection by Colletotrichum lindemuthianum was examined in susceptible and resistant French bean hypocotyls producing spreading lesions or single hypersensitive cells, respectively.

In susceptible tissue, intracellular infection vesicles formed in epidermal cells, which remained alive. Intracellular primary hyphae developed from the vesicles and colonized further host cells. A matrix layer separated the hyphal wall from the invaginated host plasmalemma. After a period of biotrophy lasting less than 24 h, the cytoplasm of infected cells gradually degenerated. This was associated with loss of the ability of cells to plasmolyse and to exclude tannic acid, here used as a permeability tracer with plant tissue for the first time. Loss of the ability of the tonoplast to contract and for neutral red to accumulate in the vacuole occurred later, and was considered to indicate cell death. In cultivars containing the pigment malvidin-3,5-diglucoside, loss of colour coincided with tonoplast rupture. During the development of the primary mycelium, the sequence of a brief biotrophy phase followed by gradual degeneration and death was repeated as each host cell became infected. Thus, despite the absence of tissue browning, only recently colonized cells at the edge of the infection were alive. As lesions appeared, narrower secondary hyphae grew within host cell walls. Death of host protoplasts and wall dissolution then occurred in advance of secondary hyphae.

In resistant tissue, infection vesicles were not formed, and the fungus was restricted in single hypersensitive epidermal cells. Most hyphae appeared dead, but some had normal ultrastructure.

These findings are discussed in relation to race specificity and the importance of biotrophy to successful pathogenesis by C. lindemuthianum.