Abstract
The Argentine stem weevil, Listronotus bonariensis (Coleoptera: Curculionidae) (ASW), is an economically significant pasture pest in New Zealand. The parasitoid wasp Microctonus hyperodae (Hymenoptera: Braconidae) was successfully introduced as a classical biological control (CBC) agent for ASW, with initial parasitism rates as high as 90% in some locations. While this was one of the most successful CBC systems worldwide, these parasitism rates have declined significantly, mirrored by ASW causing increasing damage.
While abiotic factors, such as climate, do not explain this decline, the onset of decline relates closely to the release date of M. hyperodae at numerous locations. From this it has been hypothesised that after sustained selective pressure since release, ASW may have evolved resistance to M. hyperodae. The reproductive modes of both insects further support this hypothesis; ASW reproduces sexually and has high genetic diversity, while M. hyperodae reproduces asexually and is unable to evolve at the same speed to combat any developed resistance.
Despite the suggestion of a genetic basis for this resistance, there has been limited research into what this might involve. Parasitism resistance that has been characterized in other insect species is often mediated by changes that act as a barrier to parasitism, preventing the parasitoid attacking the host, or act after parasitism as an immune response to the parasitoid egg. This thesis aimed to use transcriptomics to investigate the potential of a genetic basis for resistance in ASW, and to increase our understanding of M. hyperodae and ASW biology.
Transcriptomic comparisons were performed between ASW populations with declining and stable parasitism rates to investigate the potential of resistance involving a barrier to parasitism. Small differences were detected between ASW from either location, but location-specific responses to parasitoid exposure or attack were limited. These analyses found no evidence of a genetic resistance mechanism acting as a barrier to parasitism, consistent with previous work. The absence of a resistance mechanism here suggests parasitism decline may be a result of an alternate resistance mechanism, such as one acting after parasitism, or possibly post-release fitness decline in M. hyperodae.
Transcriptomic and genomic analyses of M. hyperodae also characterized several valuable traits that influence its success as a biocontrol agent. Firstly, a novel virus carried by M. hyperodae and transmitted to ASW during parasitism was detected. Alongside RNA sequencing of M. hyperodae venom and ovaries, this discovery improves our understanding of the parasitism complement injected into ASW, as well as the transcriptomic response of ASW to parasitism. The same data also allowed for investigation of meiosis-specific gene expression, with highest expression of these genes in the ovaries suggesting conserved function of these genes. This supports other evidence that M. hyperodae parthenogenetic reproduction involves meiosis and is therefore facultative.
Overall, this thesis has greatly expanded our understanding of M. hyperodae, ASW, and interactions between the two species. Findings from this thesis, as well as the pipelines developed for genomic and transcriptomic analyses, should be valuable in any ongoing investigation of parasitism resistance in this biocontrol system, which is critical in ensuring ASW is not released from suppression.