Elizabeth English
Graduate Student
e-mail: ede8@pitt.edu
twitter: EliseTweetsBio
B.S. in Molecular and Cell Biology from University of Connecticut, 2011
Research interests: Host-pathogen interactions, host immune system evasion, speciation of pathogens and their hosts, co-evolution of hosts and pathogens, evolution of virulence, evolution of successful pathogens, avirulence as a transmission strategy, parasitology, virology, bacteriology, and more!
Publications:
Adomako-Ankomah Y*, English ED*, Danielson JJ, Pernas LF, Parker ML, Boulanger MJ, Dubey JP, Byle JP. Host Mitochondrial Association Evolved in the Human Parasite Toxoplasma gondii via Neofunctionalization of Gene Duplicate. (2016) Genetics. Early Online. doi: 10.1534/genetics.115.186270 Link to open access article. (* These authors contributed equally)
Review: English ED, Adomako-Ankomah Y, Boyle JP. Secreted effectors in Toxoplasma gondii and related species: determinants of host range and pathogenesis? (2015) Parasite Immunol. 37(3):127-40. doi: 10.1111/pim.12166. Link to open access article.
Walzer KA, Wier GM, Dam RA, Srinivasan AR, Borges AL, English ED, Herrmann DC, Schares G, Dubey JP and Boyle JP. Hammondia hammondi harbors functional orthologs of the host-modulating effectors GRA15 and ROP16 but is distinguished from Toxoplasma gondii by a unique transcriptional profile. Eukaryot Cell. 13(12):1507-18. doi: 10.1128/EC.00215-14. Link to open access article.
Graduate Student
e-mail: ede8@pitt.edu
twitter: EliseTweetsBio
B.S. in Molecular and Cell Biology from University of Connecticut, 2011
Research interests: Host-pathogen interactions, host immune system evasion, speciation of pathogens and their hosts, co-evolution of hosts and pathogens, evolution of virulence, evolution of successful pathogens, avirulence as a transmission strategy, parasitology, virology, bacteriology, and more!
Publications:
Adomako-Ankomah Y*, English ED*, Danielson JJ, Pernas LF, Parker ML, Boulanger MJ, Dubey JP, Byle JP. Host Mitochondrial Association Evolved in the Human Parasite Toxoplasma gondii via Neofunctionalization of Gene Duplicate. (2016) Genetics. Early Online. doi: 10.1534/genetics.115.186270 Link to open access article. (* These authors contributed equally)
Review: English ED, Adomako-Ankomah Y, Boyle JP. Secreted effectors in Toxoplasma gondii and related species: determinants of host range and pathogenesis? (2015) Parasite Immunol. 37(3):127-40. doi: 10.1111/pim.12166. Link to open access article.
Walzer KA, Wier GM, Dam RA, Srinivasan AR, Borges AL, English ED, Herrmann DC, Schares G, Dubey JP and Boyle JP. Hammondia hammondi harbors functional orthologs of the host-modulating effectors GRA15 and ROP16 but is distinguished from Toxoplasma gondii by a unique transcriptional profile. Eukaryot Cell. 13(12):1507-18. doi: 10.1128/EC.00215-14. Link to open access article.
Determining the impact of MAF1 gene duplication and diversification on Toxoplasma virulence
Following invasion of the host cell, Toxoplasma gondii associates with host mitochondria. Host mitochondrial association (HMA) has been observed for quite some time, but it is only recently that the parasite factor responsible for this phenotype has been discovered (mitochondrial association factor 1; MAF1). Interestingly, the MAF1 gene is actually duplicated, and copy number varies by strain (2 or more copies in a row). My work, along with other members of the lab, has shown that MAF1 is not only duplicated, but also diversified. Upon further investigation we found that not all copies of MAF1 are able to mediate HMA. We also examined MAF1 copy number and diversification in closely related parasitic species Hammondia hammondi and Neospora caninum, and find that H. hammondi has 2 copies of MAF1 which have diversified, while N. caninum has only 1 copy of MAF1. Using cross-species complementation to assess functionality of several MAF1 copies from multiple species, we have determined that HMA evolved by neofunctionalization of an ancestral MAF1 gene. Furthermore, expression of an HMA competent copy of MAF1 in parasites that do not normally associate with host mitochondria provides a competitive advantage in vivo. This work has recently been accepted for publication and is available Early Online at Genetics.
Figure 1: MAF1 with mutated beta strands is still able to mediate HMA. Parasites that do not normally associate with host mitochondria expressing a mutant form of MAF1 (HA-tagged; green). Host mitochondria are visualized by immunofluorescence in red (MTCO2 is a mitochondrial marker). This mutant is still able to mediate HMA, as seen by the ring of red (yellow co-localization in the merge) surrounding the parasites inside the host cell.
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I am currently focused on two MAF1-related projects in the lab. In collaboration with the Boulanger Lab at the University of Victoria, I am conducting structure based mutational analysis to determine the portions of the MAF1 protein necessary to mediate HMA (Figure 1). I am also examining the impact of MAF1 expression in vivo throughout the lifecycle of the parasite, particularly during the chronic stages of T. gondii infection (Figure 2).
Preliminary data shows that when an HMA competent MAF1 copy is expressed in parasites that do not normally exhibit HMA, chronically infected mice have more cysts than mice infected with the wildtype parasites. This suggests that MAF1 plays a role in the establishment or maintenance of chronic T. gondii infection. I am currently investigating whether mice infected with HMA+ parasites have a different cytokine expression profile during chronic infection than mice infected with HMA- parasites, and what role those cytokines might be playing during chronic infection with HMA+ parasites.
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Outside the lab I spend most of my time practicing yoga or taking care of my definitive hosts. I am a huge fan of hockey (Let's go Flyers!) and ice skating, especially outdoors during the winter. I also enjoy playing board games, going out to eat, and gardening.
Somewhere between nested and flying pigeon, on a trail in Schenley Park!
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An intense game of Seven Wonders. I won by investing in science!
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Left: Neso, Right: Thebe. Their life is hard.
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