Swapnalee Sarmah, Ph.D.

Research Assistant Professor

(317) 274 7202


Alcohol exposure during prenatal development leads to neurodevelopmental abnormalities and multiple organ deformities, including heart and eye defects, collectively termed as fetal alcohol spectrum disorder (FASD). Various congenital heart defects (CHDs) are present in FASD patients, but the mechanisms of alcohol-induced cardiogenesis defects are not known. Nutritional and other environmental factors contribute to FASD severity, and how nutritional levels affect ethanol-induced birth defects represents another significant knowledge gap. The long-term goal of my research is to elucidate the mechanisms of ethanol-induced developmental defects, particularly heart defects, and to identify strategies to mitigate these defects. I have utilized a multi-disciplinary approach combining zebrafish embryology, cell labeling, and live imaging with molecular techniques to develop several lines of research to understand mechanisms of FASD.

Heart development requires contributions from multiple cardiac progenitors. Cardiac tissues are derived from the first heart field (FHF), second heart field (SHF), and cardiac neural crest cells (CNC). Interfering with any of these progenitor populations leads to heart defects. Specific interactions between FHF, SHF and CNC progenitors are required for functional valve morphogenesis, which is tightly regulated by gene networks that coordinate spatiotemporal morphogenesis mechanisms. These networks are conserved across vertebrate species, from zebrafish to human. We showed that zebrafish embryos exposed to ethanol during distinct cardiogenic events produced endocardial cushion (precursor of the heart valve) and chamber morphogenesis defects. Folic acid supplementation rescued ethanol-induced developmental defects, including endocardial cushion defects. Current research is focused on understanding how ethanol interferes with the differentiation and incorporation of different cardiac progenitors into the heart.


Postdoctoral Research Fellow, Vanderbilt University Medical Center, Nashville, TN.

Ph. D. in Chemical Sciences, Tezpur University, India.

M.Sc. in Chemistry, Gauhati University, India.

Publications & Professional Activity

Sarmah, S., Muralidharan, P., and Marrs J. 2016. Embryonic ethanol exposure dysregulates BMP and Notch signaling, leading to persistent atrio-ventricular valve defects in zebrafish. PLOS ONE 11: e0161205.

Sarmah, S., Chism, G. W., Vaughan, M. A., Muralidharan, P., Marrs J. A. and K. A. Marrs. 2016. Using Zebrafish to Implement a Course-Based Undergraduate Research Experience (CURE) to Study Teratogenesis in Two Biology Laboratory Courses. Zebrafish 13: 293-304.

Muralidharan, P., Sarmah, S., and J. A. Marrs. 2015. Zebrafish retinal defects induced by ethanol expousure are rescued by retinoic acid and folic acid supplement. Alcohol 49: 149-163.

Sarmah, S., and J. A. Marrs. 2013. Complex cardiac defects after ethanol exposure during discrete cardiogenic events in zebrafish: Prevention with folic acid. Developmental Dynamics 242: 1184-1201.

Sarmah S., Muralidharan P, Curtis C, McClintick J. N, Buente B, Holdgrafer D, Ogbeifun O, Olorungbounmi O, Patino L, Lucas R, Gilbert S, Groninger E, Arciero J, Edenberg H. J., and J. A. Marrs. 2013. Ethanol exposure disrupts extraembryonic microtubule cytoskeleton and embryonic blastomere cell adhesion, producing epiboly and gastrulation defects. Biology Open 2: 1013-1021.

Clendenon, S. G., Sarmah, S., Shah, B., Liu, Q., and J. A. Marrs. 2012. Zebrafish cadherin-11 participates in retinal differentiation and retinotectal axon projection during visual system development Developmental Dynamics 241: 442-454.

Liu, Q., M. R. Dalman, S. Sarmah, S. Chen, Y. Chen, A. K. Hurlbut, M. A. Spencer, L. Pancoe and J. A. Marrs. 2011. Cell Adhesion Molecule Cadherin-6 Function in Zebrafish Cranial and Lateral Line Ganglia Development. Developmental Dynamics 240: 1716-26.