Abstract
Obligate parasitism is defined, and the principles involved in host–parasite interactions are briefly described. In the absence of host tissue, the germination and development of rust uredospores stops with the formation of infection structures. Interaction with the host results in further development of the parasite. It has been shown that in rust-infected tissue there are increases in respiration rate, in the activity of the pentose phosphate pathway, and in the concentrations of many constituents, including RNA and auxin. Such studies have usually been conducted at relatively late stages in disease development, but there is evidence to indicate that critical interactions between host and parasite occur very shortly after inoculation. Valuable insight has recently come from electron microscope and other cell-biological studies in the early stages of the establishment of rust infections. In particular, quantitative cytophotometry has demonstrated an apparent decrease in histones and an increase in RNA in the mesophyll nuclei of rust-infected wheat leaves 48 h after inoculation. Studies on the effect of actinomycin D on the development of flax rust also point to the rapidity with which host–parasite interactions occur. This antibiotic (2.5 mg/l) does not inhibit uredospore germination. It does inhibit the development of rust infections on the host, but only if the treatment is given before 5 or 6 h after inoculation. Treatment after this stage is not effective.Attention is drawn to the possible importance of the apparent absence of nucleoli in uredospore nuclei and to the possibility that uredospore germination and the differentiation of infection structures may occur without the formation of new ribosomes. It is also suggested that successful establishment of obligate fungal parasites or their hosts may involve the derepression of host DNA and the synthesis of new proteins.