Rebecca D. Burdine

Professor of Molecular Biology
Office Phone
Guyot Hall, M159


Using zebrafish to study development and disorders


In my laboratory we are using the zebrafish to study how the left-right (LR) axis and pattern is established. Vertebrates appear bilaterally symmetric, but have internal asymmetries along the LR axis. This axis is revealed by the asymmetric placement of organs along the midline. For example, the human heart is located on the left of the body cavity, while the liver is located on the right. While genes implicated in LR patterning have been identified, we do not know how the LR axis is established, how the axis is aligned with the existing dorsal-ventral and anterior-posterior axes, or how LR information is received and interpreted by developing organs. Proper LR axis formation is critical for organogenesis as correct organ placement allows for proper connectivity with the developing vasculature. In humans, defects in LR patterning often manifest as congenital heart disease. Our current studies focus on the mechanisms of left-right patterning, and on identifying new genes involved in this process. Additionally, we use our work in zebrafish to understand human disorders including ciliopathies, RASopathies, idiopathic scoliosis and congenital heart defects.

Left-Right Patterning in the Vertebrate Embryo

Asymmetric expression of the Nodal inhibitor dand5 (magenta) in the zebrafish ciliated (green) left-right organizer.

We use the zebrafish to study how the left-right (LR) axis is established. Vertebrates appear bilaterally symmetric, but have internal asymmetries along the LR axis, as revealed by the asymmetric placement of organs. For example, the human heart is located on the left of the body cavity, while the liver is located on the right. Defects in LR patterning can lead to birth anomalies, including congenital heart defects, that are often fatal. Current models propose cilia driven flow is required to establish LR patterning, but we still lack a full understanding of how flow is translated into a signal that is understood and responded to by relevant cells to produce asymmetric gene expression in the embryo. Without a full understanding of the genes involved and the signaling pathways utilized, we are missing important information about a process that contributes substantially to congenital heart defects in humans.  Our current studies focus on identifying new players in LR patterning that will help define the pathway downstream of flow that produces asymmetric gene expression.

Selected Publications: 

Understanding how organs obtain asymmetric positions

How an organ obtains its final asymmetric position is not well understood. Organs such as the heart and pancreas form at the midline and obtain asymmetric positions later in development. Asymmetry is governed by the left-sided expression of Nodal early in development, yet each organ responds differently to this signal; for example, the heart loops to the right, while the liver is positioned on the left. To better understand how organs respond to asymmetric information, we are investigating how the developing heart responds to Nodal.  Our current studies focus on implementing genomic approaches to identify Nodal-induced transcriptomic changes that drive asymmetric organ morphogenesis.  Using confocal imaging, we take advantage of the transparency of zebrafish embryos to image asymmetric heart development in real time to better understand the collective cell movements that occur in this process. These studies additionally shed light on cell migration mechanisms that can be utilized by cancer cells to metastasize.

Selected Publications: 

Utilizing Zebrafish as a Model to Study Human Disease 

Zebrafish are an excellent model for studying human disease, in part thanks to their genetic similarity to humans, their ability to be easily manipulated biologically and chemically, and their transparency which allows for feasible observation of disease progression. Variants of unknown significance from patient whole genome sequencing can often be rapidly evaluated in zebrafish providing information critical for correct diagnoses. We have developed models to study genes involved in ciliopathies, idiopathic scoliosis, and RASopathies. Our studies provide insights into disease mechanisms, can identify potential therapeutic targets, and can enable screening of drug libraries for novel drug interventions.

Selected Publications:            


Rebecca Burdine is a faculty member in the Department of Molecular Biology at Princeton University. Her lab focuses on understanding the developmental mechanisms that control left-right patterning and organ morphogenesis in order to understanding how structure birth anomalies arise. She was named the 44th Mallinckrodt Scholar for the Edward Mallinckrodt Jr. Foundation, and received a Scientist Development Career Award from the American Heart Association in 2003. She was elected as fellow to the American Association for the Advancement of Science (AAAS) in 2018. She is currently serving on the Board of The International Society of Differentiation, and previously served on the boards of the Genetics Society of America and the International Zebrafish Society. She is on the Editorial board for Zebrafish, and regularly serves on grant review panels for the NIH and NSF. 

Dr. Burdine graduated summa cum laude from Western Kentucky University, majoring in Recombinant Gene Technology with a minor in Chemistry. She received her Ph.D. from Yale University for her thesis work with Dr. Michael Stern. Dr. Burdine carried out her postdoctoral research in the laboratory of Alexander F. Schier (Harvard) when he was at the Skirball Institute of Biomolecular Medicine at New York University. 

Dr. Burdine is a parent to a child with Angelman Syndrome. She first served on the Angelman Syndrome Foundation (ASF) scientific advisory committee in 2007 by invitation from Dr. Joe Wagstaff. She has previously served as Chief Scientific Officer for the Pitt-Hopkins Research Foundation and for the Foundation for Angelman Syndrome Therapeutics. She is currently serving on the Board of Directors and the Chair of the Science Advisory Committee for the ASF.

Honors & Awards

  • 2024 Elected member of the SDB Academy, Society for Developmental Biology
  • 2024 Clio Hall Award for Contributions to Graduate Student Professional Development at Princeton
  • 2018 Elected Fellow to the American Association for the Advancement of Science (AAAS)
  • 2016-2017 National Academies Education Mentor in the Life Sciences
  • 2013-2014 National Academies Education Fellow in the Life Sciences
  • 2012 Invited Speaker for Yale University Biology Alumni Reunion
  • 2011 Invited Speaker for NICHD National Advisory Meeting as an ARRA Success Story
  • 2003-2006 44th Mallinckrodt Scholar, Edward Mallinckrodt Jr. Foundation
  • 2003-2006 Scientist Development Award, American Heart Association
  • 2001-2002 American Heart Association Postdoctoral Fellowship
  • 1998-2001 Damon Runyon Cancer Research Foundation Fellowship
  • 1997 Selected speaker Yale Graduate Student Research Symposium
  • 1997 Anna Fuller Fund Fellowship in Molecular Oncology
  • 1991-1996 Howard Hughes Medical Institute Predoctoral Fellow
  • 1989 Department of Biology Scholarship, Western Kentucky University
  • 1988 Phi Eta Sigma Honor Society (Induction)
  • 1987-1990 President’s Honor List (3.8-4.0 GPA), Western Kentucky University
  • 1987-1990 Western Kentucky University Regents Scholarship
  • 1987 Florence and Basil C. Cole Scholarship, Western Kentucky Un


  • Ph.D., Yale University
  • B.S., Western Kentucky University

Selected Publications