Abstract:
Although the life cycle of the smut disease caused by Ustilago maydis has been known for a long time, little is known of the ultrastructural histopathology of the host-pathogen relationship.<br><br> The aim of this study therefore, was to investigate some aspects of the ultrastructural histopathology of the life cycle of U. maydis. This concerns those processes which take place after germination of the teliospores up to the formation and development of the teliospores in galls in the host.<br><br> Germinating teliospores grown on potato dextrose agar were prepared for transmission- and scanning electron microscopical studies. The following sequence of events was observed. During the initial stage of teliospore germination an increase in the size and number of lipid droplets were observed. Concomitant with this, structural changes occurred in the walls of the teliospores.<br><br> The host plant was infected with germinating teliospores and the host-pathogen relationship was studied by transmission- and scanning electron microscopy. The sporidia germinate and penetrate meristematic tissue of Z_. mays. The hyphae develop intercellularly in the middle lamellae of cell walls as well as intracellularly in the cell cytoplasm. This penetration of the hyphae into the host occurs without any significant damage to the cells. In the initial stages of gall formation, hypertrophy and hyperplasia were detected. By the use of the polyethylene glycol embedding procedure in SEW studies the development of the teliospores could be seen in the mucilage which accompanies gall formation in the plant tissue. This was followed by the disintegration of the mucilage mass during maturation of the gall. The host epidermis forms an enclosing layer of cells covering the gall which bursts when mature with subsequent the release of the teliospores.<br><br> The possible functional changes in the photosynthetic system of the host during the infection cycle were monitored with the chlorophyl fluorescence test. This test allowed the differentiation between susceptible and resistant maize plants, since the photosynthetic system of the susceptible plants showed decreased activity much sooner after infection than that of the resistant plants. The damage to the photosynthetic system was detected before any macroscopic symptoms were visible. A parallel could be drawn between the fluorescence tests and the ultrastructural observations. It was found that the damage to the photosynthetic apparatus occurred in parallel with the anatomical and morphological changes of the chloroplasts.
