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Fusarium ear blight (FEB), caused by several Fusarium species is a worldwide disease of wheat and other small grain cereals. This disease can greatly reduce grain yield and is of concern because of the potential accumulation of mycotoxins in the grain intended for human and animal consumption. Control of the disease with fungicides is variable. Inconsistency of fungicide control has been linked to the difficulty of timing treatment application. ~- • Microencapsulation of fungicide may provide a way to overcome this problem. Microencapsulated formulations were therefore assessed under controlled conditions and in a field trial. Results obtained in the growth room were promising. Work on formulation showed that the addition of the sticker Bond substantially improves the level of control of the formulation. However, under field conditions, the microencapsulated fungicide did not give any control. In vitro work showed the release of tebuconazole from the yeast capsules is by diffusion rather than by cell fracture. Screening of bacteripl isolates for the biological control of FEB also showed potential under controlled conditions but results obtained in growth room trials did not transfer to the field. Work undertaken to develop an integrated strategy for the control of FEB was unsuccessful. Compatibility problems between the formulated biological agent Botokiller and the microencapsulated formulation Micap 21.7% were observed and when applied in a dual application strategy, they did not improve FEB control ;- compared to the fungicide used alone. The use of a moderately resistant cultivar did not improve the level of control of fungicides in terms of visual symptoms and yield. However, DON contamination was markedly reduced by the application of Micap 21.7% and Folicur on the moderately resistant cv. Centrum.

Tuta absoluta is an economically significant pest of tomatoes, which has undergone a rapid expansion in its range during the past six years. One of the main means of controlling this pest is through the use of chemical insecticides including pyrethroids and spinosad. However, their intensive use has led to the development of resistance. The aim of this PhD was to understand the mechanisms underlying resistance to pyrethroids and spinosad. The target site of pyrethroids, the sodium channel, was cloned and three known knockdown resistance mutations, L1014F, M918T and T929I were found. High-throughput diagnostic assays were developed and the prevalence of the three mutations was then assessed. All three mutations were found at high frequencies in populations across the range of T. absoluta. Additionally, a fourth novel mutation L925M was found in 14% of samples. Therefore, pyrethroids are unlikely to be effective at controlling T. absoluta. Bioassays were conducted to determine the sensitivity of five populations of T. absoluta to spinosad. One population, from an area where control failure using spinosad was reported in 2012, exhibited a high level of resistance after selection in the laboratory with spinosad. Synergist bioassays did not show enhanced activity/expression of P450s and esterases. The transcriptome of T. absoluta was sequenced and used, in combination with degenerate PCR, to identify the target site of spinosad, the nicotinic acetylcholine receptor (nAChR) a6 subunit. Analysis of Taa6 revealed that two mutually exclusive exons (3a and 3b) that encode loop D of the ligand binding domain are both absent in all transcripts from the selected strain. Additionally, QPCR showed that a6 is down regulated in both larvae and adults of the selected strain. Taken together this study has provided new data on the molecular basis of resistance of T. absoluta to pyrethroids and spinosad.

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