PEOPLE
Assistant Professor
B.S. - University of North Carolina-Chapel Hill (2001-2005)
M.S. - New York University (2006-2007)
Ph.D.- University of North Carolina- Chapel Hill (2007-2013)
Post-Doc - Harvard Medical School/Brigham and Women's Hospital (2014-2019)
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Ph.D.Student
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A.S.: Corning Community College (2016-2018)
B.S.: Rochester Institute of Technology (2018-2020)
Post-Bac: Prep Program, Boston University (2020-2021)
PhD: Department of Biochemistry and Cell Biology, Boston University, (2021-Present)
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Thesis Research: Viruses are obligate intracellular parasites that depend on the host cell's translation machinery to produce viral proteins. While many viruses co-opt this machinery in well-characterized ways, the mechanisms used by negative sense RNA viruses (NSVs) remain poorly understood. NSVs generate mRNAs that are capped, polyadenylated, and monocistronic - features that make them appear nearly identical to host transcripts. Because of this, it has long been presumed that NSV mRNAs are translated via canonical host translation pathways. However, emerging evidence suggests these viruses may use non-canonical or alternative mechanisms to initiate translation. My research seeks to investigate how NSV mRNAs are selectively translated during infection, using a combination of biochemical, molecular, virological, and imaging approaches.
Photo to come
Ph.D.Student
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B.S.: University of Massachusetts, Boston (2016-2020)
Research Technician: Dana-Farber Cancer Institute, Beroukhim Lab (2020-2022)
PhD: Department of Biochemistry and Cell Biology, Boston University (2022-Present)
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Thesis Research: eIF3 is a thirteen subunit translation initiation factor whose main function is thought to be bridging mRNAs and 40S subunits. As research into eIF3 progresses, it is becoming clear that these individual subunits or subunit subcomplexes have specific functions ranging from alternative cap-binding, to regulation of ribosome content. Interestingly, upon loss of any eIF3 subunit, rates of near-cognate start codon recognition increase. I am interested in uncovering the mechanism of how this happens, and what the consequences of it may be.
Ph.D.Student
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B.S.: Montana State University (2017-2018)
B.S.: University of North Florida (2018-2021)
Post-Bac: University of North Florida, Tahimic Lab (2021-2023)
PhD: Department of Biochemistry and Cell Biology, Boston University, (2023-Present)
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Thesis Research: Canonical translation initiation requires the eIF4F complex for mRNA activation. The eIF4F complex has three subunits – eIF4E1 (cap-binding protein), eIF4G1 (scaffolding protein), and eIF4A1 (RNA helicase). In canonical translation initiation, eIF4E1 binds the m7GTP mRNA cap to recruit eIF4G1 and the rest of the canonical initiation factors. However, we know that in the absence of eIF4E1 or eIF4G1, there is a residual amount of translation occurring. My research primarily focuses non-canonical or alternative methods of translation initiation that are eIF4E1- or eIF4G1-independent.
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Photo to come
Anne Aldrich
Research Technician
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