Rachel T. Cox

Ph.D.

Department of Primary Appointment:
School of Medicine
Biochemistry
Title
Associate Professor (Tenured)
Location: Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Mechanisms governing mitochondrial function in vivo
Office Phone

Education

B.A. in Biology, University of Pennsylvania, Philadelphia, PA
Ph.D. in Genetics and Molecular Biology, University of North Carolina - Chapel Hill, Chapel Hill, NC
Postdoctoral Fellow, Department of Embryology, Carnegie Institute for Science, Baltimore, MD

Biography

Dr. Cox obtained her Ph.D. from the Curriculum in Genetics and Molecular Biology at University of North Carolina – Chapel Hill in 1992. She carried out her thesis work in the laboratory of Dr. Mark Peifer where she used the model organism Drosophila melanogaster to uncover how the highly conserved protein Armadillo/beta-catenin functions in cell-cell adhesion and cell signaling during development. After a year as a postdoctoral fellow in the Peifer lab, she went on to do a postdoctoral fellowship in the laboratory of Dr. Alan Spradling in the Department of Embryology, Carnegie Institute for Science in Baltimore, MD. There, she began studying the molecular mechanisms governing mitochondrial movement and function during Drosophila oogenesis. In 2008, Dr. Cox obtained an independent tenure track position at Uniformed Services University in the Department of Biochemistry and Molecular Biology where she continues her research on mitochondrial function and quality control during development and disease.

Career Highlights: Positions, Projects, Deployements, Awards and Additional Publications

Helen Hay Whitney Postdoctoral Research Fellowship, 1999-2002

Hébert School of Medicine Faculty Impact Award, 2015

Hébert School of Medicine Faculty Impact Award, 2017

Outstanding Biomedical Educator Award, 2018

Representative Bibliography

Saoji, M., and Cox, R. T., Mitochondrial RNase P complex in animals: mt:tRNA processing and links to disease. In RNA Metabolism in Mitochondria; Cruz-Reyes, J. and Gray, M. W., Editors; Springer-Verlag Berlin Heidelberg: Berlin, Germany, 2018; in press.

Sen, A. and Cox, R. T., Fly Models of Human Diseases: Drosophila as a Model for Understanding Human Mitochondrial Mutations and Disease. In: Leslie Pick, editor, Current Topics in Developmental Biology, Vol. 121, Burlington: Academic Press, 2017, pp. 1-27

Sen, A., Karasik, A., Shanmuganathan, A., Mirkovic, E., Koutmos, M., and Cox, R.T. (2016) Loss of the mitochondrial protein-only Ribonuclease P complex causes aberrant tRNA processing and lethality in Drosophila. Nucleic Acids Research 44(13):6409-6422

Sen, A. and Cox R. T. (2016) Clueless is a conserved ribonucleoprotein that binds the ribosome at the mitochondrial outer membrane. Biology Open 5(2):195-203. paper featured with cover image

Sen, A., Kalvakuri, S., Bodmer, R. and Cox R. T. (2015) Clueless, a protein required for mitochondrial function, interacts with the PINK1-Parkin complex. Disease Models & Mechanisms 8(6): 577-589. paper featured with cover image

Sen, A., Damm, V. T., and Cox R. T. (2013) Drosophila clueless is highly expressed in larval neuroblasts, affects mitochondrial localization and suppresses mitochondrial oxidative damage. PLoSONE. 8(1): e54283.

Cox, R. T. and Spradling, A. C. (2009) clueless, a conserved Drosophila gene required for mitochondrial subcellular localization, genetically interacts with parkin. Disease Models & Mechanisms 2(9/10): 490-499.