Naomi Gunawardena

Undergraduate Degree: BS
Undergraduate Degree Year: 2013
Undergraduate Institution: Carnegie Mellon University
Undergraduate Major: Biological Sciences

Academic Status
Year in Program: MS4
Graduate Program:
Research Advisor First Name: Grant
Research Advisor Last Name: Bullock
Research Title/Research Topic: Mitochondrial aconitase connects iron metabolism to oxidative phosphorylation
Current Research Description: We propose that mitochondrial aconitase inhibition caused by iron deficiency decreases flux through the electron transport chain and disrupts a signal that is required for erythroid progenitor cell transition past the iron-responsive differentiation checkpoint, thus leading to anemia. My project involves knocking down expression of mitochondrial aconitase in erythroleukemia cells and primary hematopoietic progenitor cells and characterizing the effects on erythroid differentiation and mitochondrial metabolism in order to elucidate the role of mitochondrial aconitase in this iron restriction checkpoint.

Undergraduate Honors: Carnegie Mellon University: University Honors 2013; Mellon College of Science Deanís List with High Honors (every semester) 2009 - 2013; Carnegie Mellon Mortar Board Senior Honor Society 2012 - 2013; Howard Hughes Medical Institute Undergraduate Summer Scholar 2012; HHMI Undergraduate Summer Researcher 2011; The Ellis School World Language Prize 2009; Outstanding Asian American Student Award, Highest Honor 2009; The Ellis School Chapter of the Cum Laude Society 2009 Additional: National Institutes of Health (NIH) T35 Summer Student in Hematology 2014

Student Committee Participation
Student Committee Involvement:

Grant Support
Grant Support Information:


1. Investigating the Connection Between Mitochondrial Aconitase and Erythropoietin Signaling During Iron Deficiency Anemia Using Gene Transfer Techniques.
Authors: Gunawardena N, Schrott V, and Bullock GC
Deanís Summer Research Program Poster Session, University of Pittsburgh School of Medicine. October 2014.

2. CD56 is a Bona Fide Activating Receptor for Natural Killer Cells.
Authors: Gunawardena N, Griffin P, and de Vallejo AN.
Summer Student Research Program Poster Session. Childrenís Hospital of Pittsburgh of UPMC. July 2010.


Screening of Candida albicans Mutants for Stress Phenotypes.
Authors: Gunawardena, N, Fanning S, Mitchell A
Howard Hughes Medical Institute Summer Scholar Symposium, Carnegie Mellon University. July 2012.


Vallejo AN*, Griffin P, Montag D, Nussbaum R, Gunawardena N, Studenski S. 2013. CD56 is a legitimate immune receptor regulating T and NK cell effector function, and its expression level predicts successful aging. J Immunol 190:119.18.