Vanessa Corby-Harris

Dept. of Ecology and Evolutionary Biology

Mailing address: 1041 E. Lowell St., Tucson, AZ 85721
Telephone: (520) 626- 2772
Fax: (520) 626-3522
Email: vcorby@email.arizona.edu

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Research Interests

My doctoral dissertation research was conducted at the University of Georgia with Dr. Daniel Promislow. I explored the evolutionary and ecological forces that maintain variation for resistance within and across natural host populations of the fruit fly, Drosophila melanogaster. For my postdoctoral work with Dr. Teri Markow, I’ve shifted my focus slightly to one particular type of interaction: interactions between Drosophila species and the vertically transmitted endosymbiont, Spiroplasma. Screens for Spiroplasma presence across a variety of Drosophila species reveal that these endosymbionts are unevenly distributed across Drosophila host species. Infections appear to be particularly concentrated within the repleta group, in species such as D. mojavensis, D. hydei, D. aldrichi, and D. willistoni. My overall goal, therefore, is to understand why infection is maintained in these species in particular. Do these bacteria confer a fitness benefit to these hosts?  Do they manipulate host reproduction? In comparison to uninfected host species, do infected host species mount less of an immune response? 

From the limited amount of data available, it appears that Spiroplasma can either be detrimental to the host or rather benign, depending on the species of host and the strain of bacteria. However, data on the fitness effects of Spiroplasma is somewhat limited, and so the first goal of my research is to more thoroughly characterize the fitness effects of Spiroplasma infection across a variety of Drosophila host species captured in nature that carry Spiroplasma.  From our collections, it does not appear that Spiroplasma causes obvious reproductive manipulations such as male-killing. However, I expect that other more fine-scale fitness effects will be uncovered from our assays.

The second aim of my research utilizes the wealth of species available both at our Tucson Drosophila Stock Center and at nearby collection sites to get at the question of why infections are particularly concentrated within the repleta group. Motivated by previous work suggesting that D. melanogaster are unable to recognize Spiroplasma infection, I hypothesize that Spiroplasma are present in certain species where the immune system cannot recognize the bacterium. In contrast, the immune system of species that do not carry the infection can effectively recognize and eliminate the infection.