Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

All honeybee colonies in the UK (excepting parts of Scotland and some islands) have the ectoparasitic mite Varroa destructor. Varroa acts as a vector for a range of viruses of honeybees which are transferred when the mite feeds on haemolymph (blood) from the developing pupa. The most important of these viruses is Deformed Wing Virus (DWV). We have demonstrated that mite infestation preferentially leads to amplification of a specific virulent form of DWV. In mite-exposed developing pupae this particular virus reaches levels almost 10,000 times higher than seen in the absence of the mite, despite the development of an immune response to the infecting virus. We want to understand why the virulent form of DWV observed in mite-infested colonies or mite-exposed pupae replicates to such elevated levels. Varroa-free honeybee colonies or Varroa-infested colonies will be used as a source of individual honeybee larvae, harvested and maintained in the laboratory under carefully controlled conditions. Individual larvae will be either fed or injected with a characterised virus population. The tissues and organs in which the virus replicates will be determined using exquisitely sensitive hybridisation techniques on either dissected pupae or sections. We will repeat these studies in larvae in which we have deliberately suppressed key components of the immune response by inhibiting expression of the genes Dicer and Argonaute. We will pre-expose larvae via feeding, to short RNA molecules designed to inhibit DWV replication. We will test whether DWV carries a gene that inhibits the effectiveness of RNA-based immune responses using well-established techniques. We will investigate the role of specific host genes implicated in components of the immune response or development to enhanced susceptibility to DWV-mediated disease. We will suppress individual genes of interest and then challenge larvae with known virus populations.

The publication of the full potato (S. tuberosum) genome sequence, including some 39,000 annotated genes, heralds a new era for the study of potato genetics and breeding. It is extremely important to build on new genomic resources and use them to gain a better understanding of potato traits, especially those that impact on crop productivity and quality, as well as resistance to biotic and abiotic stresses. Tools for investigating gene function in potato are sorely lacking, and currently potato scientists have few options other than to modify gene expression transgenically and look for altered phenotypes. Despite the recent advances in potato genomics, potato trait genetics lags behind that of model plants and other crops due to a paucity of ‘discontinuous’ variation due to mutation. This is a somewhat paradoxical state of affairs as potato, an autotetraploid outbreeder, contains extremely high levels of sequence variability. This project aims to use an inbred diploid species S. verrucosum, a tuber-bearing relative of the cultivated potato with which it is inter-fertile, to develop such mutant germplasm, with a particular focus on traits relating to tuberization and plant development, about which virtually nothing is known. A further goal is to utilise a novel next generation sequencing approach to identify genes corresponding to previously identified mutant phenotypes. To assist this process a high quality draft genome sequence of the wild type S. verrucosum genotype will be obtained. This activity is further justified by the very high levels of late blight resistance present in S. verrucosum, its self-compatibility and its current use as the recurrent parent in a set of crosses aimed at generating introgression lines (ILs) for potato. This project would also pave the way for developing a TILLING resource which could be used to dissect traits affecting disease resistance, crop yield and quality.

The green peach aphid (GPA) Myzus persicae is an agronomically important Pest worldwide. This aphid colonizes over 400 different plant species from more than 50 plant families and has developed resistance to all insecticides that are currently in use. Remarkably, a single GPA clone (consisting of genetically identical individuals) can colonize diverse plant species of several plant families, whilst the specialist pea aphid Acyrthosiphon pisum (for which the genome sequence is available) consists of genetically distinct races each of which colonizes different plant species of the family Fabaceae (or Leguminosae). The objective of this project is to identify mechanisms that have given GPA its impressive phenotypic plasticity. We will test the hypothesis that some gene families have adaptively expanded, offering GPA better protection to phytochemicals and insecticides. Given that genetically identical clones can exploit distinct host plants, we hypothesize that epigenetic regulation affects gene expression levels, and that certain gene members within these gene families are differentially up or down-regulated depending on exposure to host species and insecticides. This project tests an exiting new idea that adaptive gene duplication and Expansion of certain gene families has provided GPA with a versatile genetic toolbox allowing for a phenotypically plastic response through epigenetic regulation, thereby equipping this parasite with a vast evolutionary potential that could threaten future food security. We will use state-of-the-art genomics tools to compare aphid genomes and assess gene expression and DNA methylation profiles of GPA reared on diverse plant species and exposed to insecticides with different chemistries. We will then knock down the expression of specific GPA genes to study their effect on GPA adaptation to plants and insecticides. This project includes a translational component that will be taken forward in collaboration with Syngenta.

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.