BRIEF C.V.
2005 - present: MRC-funded PhD student
2005: B.A. Natural Sciences, Clare College, Cambridge University
RESEARCH INTERESTS
My work centers on an unusual male-killing bacteria/host relationship: that of Arsenophonus nasoniae in Nasonia vitripennis.
Unlike “normal” male-killers A. nasoniae:
- is inter- not intra-cellular, and is therefore not strictly inherited
- must re-invade its host each and every generation – as a result it is passed horizontally as easily as it is passed vertically.
- is found in a haplodiploid host
- can be cultured in cell free medium
The host, a parasitoid wasp, is easy to maintain and has a well characterized biology (see the Werren lab website at http://www.rochester.edu/College/BIO/labs/WerrenLab/). The bacterium is poorly understood beyond incidence. This and the features mentioned above make it an ideal system in which to study bacteria/host interactions and the genetics of male-killing.
The long term aims of my research into this system are outlined below:
- Properties of the A. nasoniae genome.
The identification of genes responsible for male-killing, and for the ability to invade and survive in a hostile host, requires improved knowledge of the properties and constitution of the Arsenophonus nasoniae genome. With respect to this, I will isolate A. nasoniae from the wild, examine the genome for the presence of extrachromosomal elements, and characterize the genome, via a combination of pyrosequencing and Sanger sequencing.
- Understanding sex specific virulence.
How do the bacteria identify the sex of their host and how does this identification lead to the activation of virulence genes? It is hypothesised that the lack of fertilisation in males is the trigger for killing, rather than ploidy or other “malesness” factors (Werren pers. comm.). To test this I will take advantage of the fact that cytoplasmic incompatibility in Nasonia produces females (i.e. fertilization has occurred) that are masculinised (i.e. haploid). Whether or not these individuals are killed by A. nasoniae will dispel or support the hypothesis.
- Characterisation of the impact of the bacterium on its female host.
The characterisation of the interaction between the male killer and the wasp involves a primarily phenotypic approach. It is important to know whether infection has a negative, neutral or positive impact on host fitness. I will use head size and fecundity as proxies for fitness and compare measurements of these variables from uninfected and infected individuals in three genetically different wasp lines.
- Coevolutionary history of bacterium and host.
Has A. nasoniae evolved in a single-species system or is it able to move between the different species of Nasonia and even to other wasp families? Making use of the ease of horizontal transfer upon superparasitism I will transfer infection from vitripennis into the other two Nasonia species and observe its effects including strength of the male killing phenotype and vertical transmission efficiency.
- Evasion of host immune system.
Do the bacteria elicit an immune response in the host or not? If a host immune response is produced, how do the bacteria evade it, and if no response is produced how do the bacteria avoid detection? I plan to use immune gene data from the vitripennis genome project and RTPCR to look at the expression levels of key immune system genes over time following infection. Key genes can be identified in the bacteria using a technique pioneered by Daborn (2001). E. coli expressing random sections of the A. nasoniae genome are injected into caterpillars and the time to clearing measured. E. coli are usually cleared quickly by the caterpillar immune system, therefore any that remain do so as a result of genes from Arsenophonus. This allows the identification of important regions of the genome, which can then be scrutinised further.
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