A cytological study of the net blotch disease of barley caused by Pyrenophora teres

• Published in: Physiological plant pathology Vol. 22; no. 3; pp. 321,IN5 - 329,IN14
• Main Authors: Keon, J.P.R., Hargreaves, J.A.
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.05.1983
• ISSN: 0048-4059
• DOI: 10.1016/S0048-4059(83)81019-4

Light and electron microscope studies were made on the penetration and infection of barley leaves by Pyrenophora teres. Both successful and abortive attempts to penetrate the epidermal cells were observed. At successful penetration sites a primary vesicle developed within the epidermal cell, followed by the formation of a secondary vesicle. Failure to breach the epidermal cell wall was associated with the formation of papillae. Subsequent to vesicle formation, in a susceptible interaction, hyphae penetrated through the lower epidermal cell wall and the colonizing hyphae developed intercellularly in the mesophyll tissue. No hyphae were seen to penetrate the mesophyll cells during the early stages of infection, although intracellular hyphae were occasionally observed in senescent cells during later stages. Initially the lesions were clearly delimited. Cells within the developing lesions exhibited various degrees of disruption. Loss of tonoplast integrity appeared to precede swelling and vesiculation of chloroplasts. In many cells complete disorganization of the internal membranes occurred and the cells collapsed. Cells exhibiting these degenerative changes were always in close contact with intercellular hyphae. Subsequent colonization was associated with chlorosis of tissue surrounding the netted lesions. The degenerative changes in cells from this chlorotic tissue were different to those observed in cells within the netted lesion and resembled those which occur during normal leaf senescence. Cells exhibiting these symptoms were not always in contact with the hyphae of the pathogen. These observations are discussed in relation to the role of contact phenomena and toxins in the pathogenesis of this disease.