Location and Contact Information
The Frankel Lab is devoted to understanding the genetic basis of neurological disorders with an emphasis on epilepsy and a growing interest in closely related synaptic disorders that include seizures, such as autism and intellectual disability. Our lab’s current focus is on better modeling epilepsy as a complex trait at the physiological and molecular level using a multidisciplinary approach—genetics, genomics, and biochemistry—in genes encoding ion channels, synaptic and RNA binding proteins. This also includes modeling severe pediatric epileptic encephalopathies in mice, as many of these disorders are of early childhood.
The lab’s work also includes collaboration with other Institute of Genomic Medicine (IGM) members in related areas and assisting Columbia’s Precision Medicine Initiative by providing oversight in mouse genetics, genomics, and biology.
Join the Frankel Lab
The Frankel Lab has opportunities for highly motivated individuals who have an interest in our research. Please email your application to Dr. Wayne Frankel at email@example.com.
Postdoctoral Research Scientist: Neurophysiology of genetic epilepsy in model systems
The research lab of Wayne Frankel, PhD, in the Institute of Genomic Medicine (IGM) and the Department of Genetics and Development at Columbia University Irving Medical Center seeks a competitive postdoctoral scientist to study neuronal activity and synaptic function in newly developed genetic models of epilepsy. We are most interested in candidates that have recent doctoral training in electrophysiological or optical whole cell recordings of neurons, in vivo or ex vivo. The position also encourages opportunity for collaborations, including but not restricted to co-mentorship by other IGM or academic faculty, and training opportunities in molecular genetics.
Competitive applicants will have completed their PhD and published one or more first-author research articles in leading journal(s). We seek candidates who are especially motivated to take advantage of this unique opportunity to advance their careers by combining their existing expertise in neurophysiology, with training in molecular genetic analysis and disease modeling.
Founded in 2015, IGM seeks to comprehensively integrate genetics and genomics into research, training, and patient care and to develop programs that prepare trainees for careers as researchers and clinicians in the expanding field of genomic medicine.
Columbia University is an equal opportunity/affirmative action employer. Women and minorities are encouraged to apply.
BS, University of California Irvine (UCI)—2016
Virginia's undergraduate research was in the Department of Neurobiology and Behavior at UCI, where she investigated the role of epigenetic mechanisms on learning and memory processes. Her interest has always been in the translational aspects of scientific research, and the Frankel Lab provides her with the opportunity to explore different therapeutic, gene-targeted approaches in genetic models of neurological diseases like epilepsy. Her work in the lab focuses on modeling gene therapy for the treatment DNM1 epileptic encephalopathy.
BSc Human Biology, University of Texas
MS Cancer Genetics, University of Texas MD Anderson
Devin's research focuses on the function and physiological consequences of loss of Celf4 in mouse models of human neuropathy. As an RNA binding protein, the Frankel Lab has demonstrated that Celf4 normally functions to regulate a vast number of targets throughout the neuron. Understanding the specific role of Celf4 in translation control is the basis of Devin's work. To this end, he and his colleagues have devised a number of models to parse when and where Celf4 normally functions and how loss of Celf4 at the synapse may contribute to disorder.
BA Biology, Boston University (2016)
Before she graduated, Ayla was a JAX Summer Student where she conducted an independent assessment of hepatic insulin resistance in a murine model for Alström Syndrome. She received her BA in biology from Boston University in 2016.
Megha Sah, PhD
Postdoctoral Research Scientist
Megha received a PhD in Neurobiology from the University of Connecticut, where her research focused on studying signaling pathways in the hippocampus, specifically the Autism associated MET – ARF6 axis at excitatory synapses and its role in dendritic spine morphogenesis. Building on her graduate work, her current research in the Frankel Lab focuses on studying epilepsy risk gene alleles and how they cause imbalance of neuronal networks in seizure disorders. More specifically, her project is centered on examining the molecular basis of epilepsy caused by mutations in non-ion channel genes IQSEC2 and ARHGEF9 with a focused goal of development of therapeutic intervention for these mutations.
Jia Jie (JJ) Teoh, PhD
Postdoctoral Research Scientist
Education and Training
BSc (Biotechnology), University Tunku Abdul Rahman, Malaysia (2006)
Msc (Cell Biology), University Tunku Abdul Rahman, Malaysia (2012)
PhD in Medical Science (Cell Biology), Osaka University, Japan (2017)
Japanese Government MEXT Scholarships 2012-2017
JJ's research interests are intracellular trafficking, brain anatomy, and imaging. He has been working with an intracellular trafficking gene (Arfgef1) since his PhD. In Arfgef1 knockout mouse brain, he observed cortical and hippocampal neuron cell death, occurring concurrently with the tangential migration of interneurons during embryonic development stages. Currently, at Columbia, he is working on two epileptic mouse models. One of them is an Arfgef1 haploinsufficiency model. He is examining the mechanism of disease by probing the endocytic cycle of the key surface receptor proteins.
BA in Neuroscience, Smith College (2017)
Wanqi received her BA in Neuroscience and Biomathematics from Smith College. During her graduate study, she hopes to provide a better understanding of the molecular mechanism of epilepsy and its comorbidities. Currently in the Frankel Lab, she is studying the Slack channel encoding gene KCNT1 and the ARHGEF9 gene encoding a brain-specific GDP/GTP-exchange factor collybistin.
Associate Research Scientist
Damian has been studying neuronal function using electrophysiology and imaging techniques throughout his research career. For his doctorate in Tom Cunnane’s laboratory in the Department of Pharmacology at the University of Oxford, Damian studied neurotransmission in sympathetic neurons. Damian’s used calcium imaging and electrophysiology to study neurotransmitter release at individual nerve terminal varicosities and nicotinic receptor-mediated modulation of sympathetic neurotransmitter release.
After his DPhil, Damian joined Stephen Ikeda’s lab at NIAAA in Bethesda, Maryland. During this postdoctoral training, Damian studied the mechanisms involved in voltage-gated calcium channel modulation. Damian also developed a method for high-efficiency heterologous proteins expression in adult primary neurons, and a method for rapid modification of proteins in live cells using an inducible protease system.
Damian continued his postdoctoral training in Amy MacDermott’s laboratory studying the physiological properties of stem cell-derived neurons. During this time and his position of managing the electrophysiology and calcium imaging section of the Columbia Stem Cell Core, Damian has gained extensive experience of stem cell-derived tissues. He has been central to projects which span across the field, including the characterization of stem cell lines, understanding the mechanisms of neuronal development and disease, and the development of drug screening platforms for ALS and neuromuscular disease.
The aim of Damian’s research is to understand functional changes in neurons that occur in epilepsy and intellectual disability. Using a variety of electrophysiological and image-based techniques, Damian can identify changes at molecular, individual neuron, and synaptic levels. This work is carried out with the Boland, Goldstein, and Frankel laboratories, using murine and stem cell-based models that harbor disease-causing genetic variants identified at the IGM. Insight into the mechanism of changes to neuron function will provide novel drug targets to specific biological processes, which has the potential to improve treatment of previously intractable disease.
Asinof S, Mahaffey C, Beyer B, Frankel WN, Boumil R. Dynamin 1 isoform roles in a mouse model of severe childhood epileptic encephalopathy. Neurobiol Dis. 2016 June 27.pil: S0969-9961(16)30154-1.
Dhindsa RS, Bradrick SS, Yao X, Heinzen EL, Petrovski S, Krueger BJ, Johnson MR, Frankel WN, Petrou S, Boumil RM, Goldstein DB. Epileptic encephalopathy-causing mutations in DNM1 impair synaptic vesicle endocytosis.
Neurol Genet. 2015, Apr 17;1(1):e4.
Asinof SK, Sukoff Rizzo SJ, Buckley AR, Beyer BJ, Letts VA, Frankel WN, Boumil RM. Independent Neuronal Origin of Seizures and Behavioral Comorbidities in an Animal Model of a Severe Childhood Genetic Epileptic Encephalopathy. PLoS Genet. 2015, Jun 30;11(6):e1005347.
Letts VA, Beyer BJ, Frankel WN. Hidden in plain sight: spike-wave discharges in mouse inbred strains. Genes Brain Behav. 2014, Jul;13(6):519-26.
Oliva MK, McGarr TC, Beyer BJ, Gazina E, Kaplan DI, Cordeiro L, Thomas E, Dib-Hajj SD, Waxman SG, Frankel WN, Petrou S. Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence epilepsy. Neurobiol Dis. 2014, Jul;67:180-90.
Wagnon JL, Briese M, Sun W, Mahaffey CL, Curk T, Rot G, Ule J, Frankel WN. CELF4 regulates translation and local abundance of a vast set of mRNAs, including genes associated with regulation of synaptic function. PLoS Genet. 2012, 8(11):e1003067.
Sun W, Wagnon JL, Mahaffey CL, Briese M, Ule J, Frankel WN. Aberrant sodium channel activity in the complex seizure disorder of Celf4 mutant mice. J Physiol. 2013, Jan 1;591(1):241-55.
Tokuda S, Mahaffey CL, Monks B, Faulkner CR, Birnbaum MJ, Danzer SC, Frankel WN. A novel Akt3 mutation associated with enhanced kinase activity and seizure susceptibility in mice. Hum Mol Genet. 2011, Mar 1;20(5):988-99.
Boumil RM, Letts VA, Roberts MC, Lenz C, Mahaffey CL, Zhang ZW, Moser T, Frankel WN. A missense mutation in a highly conserved alternate exon of dynamin-1 causes epilepsy in fitful mice. PLoS Genet. 2010, Aug 5;6(8).
Tokuda S, Beyer BJ, Frankel WN. Genetic complexity of absence seizures in substrains of C3H mice. Genes Brain Behav. 2009, Apr;8(3):283-9.
Beyer B, Deleuze C, Letts VA, Mahaffey CL, Boumil RM, Lew TA, Huguenard JR, Frankel WN. Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4. Hum Mol Genet. 2008, Jun 15;17(12):1738-49.
Yang Y, Mahaffey CL, Bérubé N, Maddatu TP, Cox GA, Frankel WN. Complex seizure disorder caused by Brunol4 deficiency in mice. PLoS Genet. 2007, Jul;3(7):e124.