Infection of Wheat and Oats byPyrenophora tritici-repentisand Initial Characterization of Resistance

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Abstract
Over a 72-hr postinoculation period, conidial germination (99%) and production of germ tubes (2.5 per conidium) by Pyrenophora triticirepentis were similar on leaves of susceptible ND 495 and resistant BH 1146 spring wheats and highly resistant Lodi oats. Approximately production was significantly greater on Lodi (2.1 per conidium) than on ND 495 (1.8 per conidium) and greater on ND 495 than on BH 1146 (1.5 per conidium), suggesting stimulation from susceptibility and from high resistance. The fungus usually entered the host epidermal cell from the appressorium with a penetration peg that subsequently developed a vesicle. Secondary hyphae formed from the vesicle and invaded the mesophyll intercellularly. Penetrations were rate 3 hr after inoculation and increasing by 6 hr, with most occurring from 12 hr on. From 24 hr on, the percentage of papilla formation around the infecting hypha was significantly greater in Lodi (29-47%) than in BH 1146 (11-13%) and greater in BH 1146 than in ND 495 (3-7%). From 12 hr on, the percentage of appressoria colonizing host cells (hyphae not covered by papillae and growing beyond initial penetration) was similar in ND 495 and GH 1146 (20-34%) and significantly lower in Lodi (4-7%). In Lodi, hyphae from successful colonizations were restricted to the intercellular area of a few epidermal and mesophyll cells, resulting in small brown leaf flecks 8 days after inoculation. Lesion size in BH 1146 was half that in ND 495, but mesophyll cells in lesions on both wheats had similar vesiculation of membranes and chloroplast degeneration. Papilla formation appeared to be an active defense against infection by P. tritici-repentis in Lodi and a much less active defense in BH 1146 and ND 495. Subsequent severe restriction of hyphal and surrounding lesion growth in Lodi and greater restriction in BH 1146 than in ND 495, without obvious histological or cytological structural mechanisms for restriction, suggest a molecular mechanism for resistance to fungal development, following infection and papilla formation, that is very active in Lodi and less active in BH 1146.