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There is evidence that wheat, as well as containing genes for resistance, also contains genes that promote susceptibility to disease. Mutagenesis of the variety Hobbit 'sib' produced a number of lines with increased resistance to yellow rust (Worland & Law, 1991). The aim of this research was to characterise the resistance of the Hobbit 'sib' mutants, to identify and map the mutations and to determine which conferred resistance. The incidence of genes promoting susceptibility in other varieties also formed part of the investigation since manipulation of these genes may enable the resistance of commercial varieties to be improved. Significantly improved resistance to yellow rust relative to Hobbit 'sib' was demonstrated in 17 of the 21 mutants investigated, confirming the previous findings of Worland & Law, 1991 (IAEA Vienna, Mutation Breeding Newsletter 38: pp2 - 5). Furthermore, resistance to brown rust and mildew was also demonstrated in a subset of mutants, with one mutant, 13-48, exhibiting high levels of resistance to all three diseases. The broad spectrum of resistance in 13-48 suggests that mutation has inactivated either a single gene for susceptibility with a common effect on all three diseases, or a number of genes for susceptibility, each specific for a different disease. No mutants were identified with significantly improved resistance to Stagonospora nodorum or Septoria tritici, suggesting that this method of inducing resistance may only be of value for obligate pathogens. Using molecular techniques, deletions were identified in 12 mutant lines, and the deletions were spread throughout the genome. Several mutant lines contained more than one deletion. "Representational Difference Analysis" was used successfully to identify deletions in selected mutants and, in contrast to using RFLP probes, provided a more targeted approach to identifying deletions irrespective of chromosome location. Analysis of the segregation of deletion markers in F2 populations segregating for disease resistance identified a deletion on 4DL of 13-48 that segregated with yellow rust and brown rust resistance. This was due to linkage in the case of brown rust resistance, but the yellow rust resistance may be due directly to the deletion, possibly as a consequence of the removal of a gene for susceptibility to this disease. A number of deletions were identified, both in 13-48 and other mutants, that did not segregate with resistance. Therefore, the deletion markers may be useful both as tags facilitating the selection of deletions conferring resistance, and also for the removal of deletions not implicated in improving resistance. The distribution of genes for susceptibility in several varieties, most of which are in commercial use, was examined using either segregational tests for allelism or backcross reciprocal monosomie analysis in order to identify targets for disease resistance improvement. Both these approaches proved to be unsuccessful. The reasons for this failure are presented and possible solutions described. The nature and possible roles of genes for susceptibility are discussed.