An extension of the code is planned to cover, in the first instance, maize and sorghum, and, subsequently, forage grasses and dicotyledonous crops, and a full version, with illustrations, will he published elsewhere. It is very much hoped that the final version will not differ significantly from that published here, but any suggestion for minor amendments or for changes in phraseology would he welcomed.

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SUMMARYHorizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genotypes (races or isolates) . If the total non-environmental variance in levels of resistance is due to main effects only (differences between cultivars and differences between isolates) the resistance and the pathogenicity (in the broad sense) are horizontal in nature . Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance component in this test due to interaction between cultivars and isolates .A host and pathogen model was made in which resistance and pathogenicity are governed by five polygenic loci . Within the host the resistance genes show additivity . Two models were investigated ; in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance . Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen .The cultivar/isolate test in model I showed only main effect variance . Surprisingly, the variance in model II was also largely due to main effects . The contribution of the interaction to the variance appeared so small, that it would be difficult to discern it from a normal error variance .So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen . The data reported so far support the idea that model II rather than model I is the realistic one .The two models also revealed that populations with a polygenic resistance based on the gene-forgene action have an increased level of resistance compared with the addition model, while its stability, as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action . Mathematical studies of Mode too support the gene-for-gene concept .The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system . All genes for true resistance in the host population, whether they are major or minor genes, are considered to interact in a gene-for-gene way with virulence genes, either major or minor, in the pathogen population .The models revealed other important aspects . Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model . The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model .The effect of a resistance gene on the level of resistance of the population consists of its effect 5 on a single plant times its gene frequency in the population . Due to the adaptive forces in both the host and...

Uredospore production per day and per sporulation period was measured under near-optimal conditions. Pustule density influenced time and rate of pustule opening, size of pustules, time of maximum sporulation, length of the sporulation period and the time and rate of tissue necrotisation. Within limits total dry weight of spores per leaf per sporulation period was independent of pustule density; it roughly equalled the dry weight of the spore producing leaf. The longest sporulation period observed was 65 days; at low pustule densities secondary pustules replaced exhausted primary pustules. Infectivity of the spores was normal up to 46 days after inoculation. The long sporulation period was epidemiologically interpreted as a survival mechanism.