Susan M. Smith, PhD
- Transcriptome Profiling Identifies Ribosome Biogenesis as a Target of Alcohol Teratogenicity and Vulnerability during Early Embryogenesis
- An evolutionarily conserved mechanism of calcium-dependent neurotoxicity in a zebrafish model of fetal alcohol spectrum disorders
- CaMKII represses transcriptionally active β-catenin to mediate acute ethanol neurodegeneration and can phosphorylate β-catenin
- Genomic factors that shape craniofacial outcome and neural crest vulnerability in FASD
- Inappropriate feeding behaviors and dietary intakes in children with fetal alcohol spectrum disorder or probable prenatal alcohol exposure
- Neural crest development in fetal alcohol syndrome
- High-throughput transcriptome sequencing identifies candidate genetic modifiers of vulnerability to fetal alcohol spectrum disorders.
Dr. Smith’s laboratory studies the molecular mechanisms by which dietary components affect prenatal development. Current work largely focuses upon ethanol and how it causes fetal alcohol syndrome. We are interested in how alcohol damages the embryo and fetus, and in the environmental and genetic factors that attenuate or heighten alcohols neurotoxicity.
First described in 1968, Fetal Alcohol Spectrum Disorders (FASD) remain a leading known cause of neurodevelopmental impairment in the U.S. Our work examines the molecular mechanism by which alcohol causes the specific neurobehavioral and cranofacial dysmorphologies that typify FASD. Our research has identified much of the intracellular signaling pathway initiated by ethanol to trigger the apoptotic elimination of craniofacial precursors, a population known as the neural crest.
These signals involve the G protein / inositide phosphate-mediated release of intracellular calcium stores, which in turn activate calcium signals including CaMKII, and the subsequent loss of nuclear ?-catenin, which is an important trophic factor for neural crest survival. We have identified two closely related chick embryo strains whose neural crest populations differ greatly in their sensitivity to ethanol-induced apoptosis. We have initiated molecular analysis to identify gene sequences that may confer sensitivity or resistance to ethanols neurotoxicity. We have also become very interested in maternal nutritional factors that modulate fetal sensitivity to alcohol. We have recently shown that a subclinical maternal iron inadequacy greatly exacerbates alcohols damage to the cerebellum and to cerebellum-dependent learning.
Graduate Student, Smith Lababrar_alshaer@unc.edu
Abrar Al-Shaer joined NRI as a research assistant in Dr. Susan Smith's lab in Summer 2017 and is pursuing her PhD in Nutrition from the University of North Carolina Chapel Hill starting August 2017. She graduated from UNC Charlotte in May 2017 with a BS in Computer Science - Bioinformatics Concentration, and Biology minor. Her previous research focused on metagenomics data analysis and statistical genomics analysis and visualization. Her research interests include nutrigenomics and metabolic pathway analysis with fetal-alcohol exposed cells and their relationships with particular nutrients.
Research Technician, Smith Labjoshua_baulch@unc.edu
Joshua received his B.S. in Biology in May of 2016 from High Point University in High Point, NC. His undergraduate research focused on the phylogenetic differences of parasitic wasps in the piedmont area. His previous work at the NRI consisted of assisting the research of the Ideraabdullah lab during the summer of 2015. He joined the NRI in September 2016 where he currently assists the Smith lab with their research of ethanol and the impacts it has upon fetal neurological growth and development.
George Flentke, PhD
Research Specialist, Smith Labgflentke@email.unc.edu
George Flentke received his Ph.D. in Biochemistry from the University of Wisconsin-Madison, where his dissertation focused on the structure and catalytic activity of the enzyme UDP-galactose-4-epimerase, which is crucial for galactose metabolism. His postdoctoral research in Biochemistry and Pharmacology at Tufts University / New England Medical School focused on the design of inhibitors of dipeptidyl peptidase enzymes, which control immune function and HIV infection. After returning to UW-Madison he continued working with the immunosupressives cyclosporine and rapamycin. He is an experienced enzymologist/protein chemist and synthetic organic chemist. Currently, he manages Dr. Smith’s lab, where he investigates the mechanism by which alcohol alters ribosomal signaling and mTOR activity in alcohol-exposed neural crest.
Doctoral Student in Nutrition, Smith Labkhelfri@live.unc.edu
Kaylee Helfrich joined the NRI as a doctoral student in nutrition in August 2016. She completed her BS degree in Biochemistry at Clemson University in December 2015. Her research focused on signaling mechanisms that controlled energy expenditure in plants. Kaylee works with Dr. Susan Smith to research prenatal alcohol exposure and its interaction with iron metabolism in the mother and infant.
Nipun Saini, PhD
Postdoctoral Research Associate, Smith Labnipun_saini@unc.edu
Nipun Saini joined the NRI in the summer of 2017 for her second postdoctoral position and will be working with Dr. Smith on fetal alcohol syndrome. She completed her PhD. in Biochemistry from University of Nebraska-Lincoln, where her dissertation was focused on the characterization of inhibitors of fatty acid transport protein-2 in cell and animal models to reduce obesity, lipotoxicity and related diseases. After earning her PhD, she moved to the North Carolina Research Campus as a postdoctoral research fellow in the Department of Biological and Biomedical Sciences at North Carolina Central University and worked on understanding the mechanism of microRNA-mediated regulation in metformin treated breast cancer cells.