Thesis (M. Ag. Sci.)--University of Adelaide, Dept. of Genetics, 1954. / Typewritten copy. Comparative study of genes for resistance to bunt (Tilletia caries (D.C.) Tul. and T. foetida (Wallr.) Liro); Cytological investigations in Phalaris called part 2.

Typewritten copy Comparative study of genes for resistance to bunt (Tilletia caries (D.C.) Tul. and T. foetida (Wallr.) Liro); Cytological investigations in Phalaris called part 2.

The purpose of this study was to investigate the ultrastructure of Tilletia caries teliospores. Specimens were prepared for viewing in the electron microscope by freeze-etching and thin-sectioning techniques. Thin-sectioning techniques gave excellent results with the teliospore walls and the lipid bodies within the teliospore but failed to adequately fix the membranes and internal organelle systems. Micrographs of Tilletia caries teliospores prepared using thin-sectioning show three major wall layers and two partition wall layers and abundant lipid bodies. The freeze-etch method of spore preparation proved superior to the thin-sectioning used in this study to reveal the internal organelle systems of the T. caries teliospore. The following anatomical details of teliospores were revealed using this technique: a multilayered spore wall, structural details of the plasma membrane, surface and cross-fractured views of the nucleus, details of the nuclear envelope, and surface and cross-fractured views of spherical bodies of unknown function.

Caryopses of wheat were studied during infection by Tilletia caries and T. controversa. Initially the pathogens penetrated embryos of the host. After the embryo tissue was consumed by the fungi, endosperm tissue was penetrated and consumed. Initial penetration of endosperm tissue was in localized areas. During infection the fungus mycelium spread intercellularly, but occasionally was seen intracellularly. As the host tissue was consumed teliospores were formed. At maturity a host cell layer 4-6 cells thick remained which retained the mature teliospores. Histochemical studies indicated that carbohydrates and lipids of the host disappeared soon after invasion by the pathogens. Nuclei and cell walls remained intact after other cell components decomposed.