Soo-Kyung Lee, Ph.D.
Associate Professor, Papé Family Pediatric Research InstituteEmail: firstname.lastname@example.org
Office: BRB 311
Soo-Kyung Lee completed her B.S. degree in Pharmacy at Chonnam National University in Gwangju, Korea. She remained at Chonnam National University where she earned her M.S. and Ph.D. degrees. In 2001, she moved to the Salk Institute in San Diego for the postdoctoral studies. In 2004, she was appointed assistant professor at the Baylor College of Medicine. Soo-Kyung came to Oregon Health & Science University in 2010 as an associated professor at the Pediatrics department with a joint appointment in the Vollum Institute.
Summary of Current Research
Unraveling the processes that generate the numerous neuronal subtypes and establish their appropriate connections to form a functional CNS is one of the main challenges in neuroscience today. Particularly, decoding the gene regulatory network responsible for neuronal subtype specification is a fundamental step toward understanding the CNS development and advancing methods to generate specific neurons in regenerative medicine.
Our goal is to develop a comprehensive map of the complex gene regulatory networks that direct cell-fate specification and assembly of neuro-circuits. Our major model systems include the spinal cord, which consists of distinct classes of neurons to assemble motor and sensory circuits, and the arcuate nucleus of the hypothalamus, which forms a core neuro-circuitry that mediates actions of peripheral adiposity-signals, leptin and insulin, for energy balance. To achieve our goals, we dissect multiple layers of gene regulatory steps that render neuronal cell-fate specification, taking the following steps; to define transcription complexes specifying each neuronal population, to identify their downstream effector genes conferring unique cell-identity, to understand epigenetic strategy orchestrating timely changes on gene transcription, to uncover the molecular mechanism by which the peripheral cues modulate neuronal gene expression, and to generate specific neuronal subtypes from stem cells by applying the developmental gene regulatory strategy that we define. Our study will eventually contribute to the design of a rational strategy to repair damaged neurons and to treat metabolic disorders in the human.
Having been pioneering studies of combinatorial transcription and microRNA codes in the spinal cord development for the past years, we have developed many molecular tools and animal model systems that enable us to explore critical layers of transcriptional regulation, such as epigenetic control, and that are applicable to investigating other areas of the CNS. We are employing combined approaches of mouse genetics and chick embryology to take advantage of their complementary strengths as experimental systems. In addition, we are utilizing embryonic stem cells extensively and biochemical and molecular methods to dissect the development of spinal and hypothalamic neurons.
Asprer JS, Lee B, Wu CS, Vadakkan T, Dickinson ME, Lu HC and Lee S-K. (2011) LMO4 functions as a co-activator of neurogenin 2 in the developing cortex. Development 138:2823-2832. PMID: 21652654.
Lee S and Lee S-K (2010) Crucial roles of histone-modifying enzymes in mediating neural cell-type specification. Current Opinion Neurobiology 20:29-36. PMID: 20137907.
Lee S, Lee B, Lee JW and Lee S-K (2009) Retinoid signaling and neurogenin2 function are coupled for the specification of spinal motor neurons through a chromatin modifier CBP. Neuron 62:641-654. PMID: 19524524.
Joshi K, Lee S, Lee B, Lee JW and Lee S-K (2009) LMO4 controls the balance between excitatory and inhibitory spinal V2 nterneurons. Neuron 61:839-851. PMID: 19323994.
Lee S, Lee B, Joshi K, Pfaff S, Lee JW and Lee S-K (2008) A regulatory network to segregate the identity of neuronal subtypes. Developmental Cell 14:877-889. PMID: 18539116.
Visvanathan J, Lee S, Lee B, Lee JW and Lee S-K (2007) The microRNA miR-124 antagonizes the anti-neural REST/SCP1 pathway during embryonic CNS development. Genes and Development 21:744-749. PMID: 17403776.