Rachel Cox, Ph.D.

Rachel T. Cox, Ph.D.

Name: Rachel T. Cox, Ph.D.

USU Department of Primary Appointment: 
Biochemistry
Title: 
Associate Professor (Tenured)
Faculty Rank: 
Associate Professor
Location: 
Uniformed Services University of the Health Sciences, Bethesda, MD

Research Interests:
Mechanisms governing mitochondrial function in vivo

Office Phone: 
(301) 295-9791

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.

Representative publications, projects, and/or deployments

  • 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

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.