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Bates Lab

Dr. Emily Bates uses genetics to determine the molecular mechanisms of pediatric disorders.  Her research has identified mutations in a gene that cause migraine headaches and has identified a likely target for alcohol that causes Fetal Alcohol Syndrome.

Mechanisms of Disease
As the first step to finding potential therapeutics, Dr. Emily Bates uses genetics to determine molecular mechanisms of pediatric disorders.  Clues into common pathology can start from human genetic disorders.  Two focused genetic research projects led to applications that will likely impact some of the most common pediatric disorders. Early stages of these studies include finding genetic mutations responsible for pediatric disorders.

Fetal Alcohol Syndrome: It has long been known that prenatal exposure to alcohol can cause cognitive impairment and increased incidence of physical birth defects.  Despite counseling against alcohol consumption during pregnancy, fetal alcohol spectrum disorder (FASD) continues to affect 2-5% of some populations and is the leading known cause for mental retardation in the Western world. In the most severe cases, known as fetal alcohol syndrome (FAS), bone structures fail to fuse and facial features are abnormal.  Despite a great need to treat FAS, the direct mediator of the alcohol's affect on developmental signaling has been unknown.

The Bates lab identified a potential therapeutic target for fetal alcohol syndrome by studying a rare genetic disorder that has the same spectrum of congenital birth defects as FASD.  The genetic disorder, (Andersen Tawil Syndrome) is caused by genetic disruption of a potassium channel. This potassium channel controls the gradient of ions across the cell membrane.  The same potassium channel is blocked in the presence alcohol.  The Bates lab now explores the possibility that the potassium channel can be altered to prevent the devastating affects of alcohol on a developing baby.

Migraine: Migraine is a complex episodic neurological disorder that often includes aura, headache, nausea, and hypersensitivity to sensory stimuli like light, sound, pressure, and heat.  The Bates lab asks how migraine occurs using clues from human genetics.  The Bates lab also tests potential therapies using mice as a model (her studies were recently highlighted on National Public Radio (NPR).

Mechanisms of Healthy Development and Repair: From the time of conception, a single cell divides and gives rise to many different cell types in organs that perform specialized roles in a fully functional animal.  The Bates lab asks how cell fate is determined. The Bates lab recently found that changing the function of a potassium channel affects cell fate decisions. This is exciting because ion channels are readily targeted pharmacologically. This presents the possibility that ion channels could be manipulated to influence cell fate choices to generate specific tissues like cartilage or bone. For these potential applications, the Bates lab explores the role of ion flux in cell fate decisions.

DahalGiri 206 x 156.jpg Giri Dahal, PhD, Postdoctoral Fellow
Research Project:  Mechanisms underlying Andersen-Tawil Syndrome and the developmental function of a potassium channel.
RoseSteven 206 x 156.jpg Steven Rose, BS, Research Assistant

Brennan KC, Bates EA, Shapiro RE, Zyuzin J, Hallows WC, Huang Y, Lee HY, Jones CR, Fu YH, Charles AC, Ptáček LJ (2013) Casein Kinase Iδ mutations in familial migraine and advanced sleep phase. Science Translational Medicine-May 1;5(183):183ra56.

Bates EA (2013) A potential molecular target for morphological defects of fetal alcohol syndrome: Kir2.1.  Current Opinion in Genet Dev, Jun;23(3): 324-99.

Dahal GR, Rawson J, Gassaway B, Kwok B, Tong Y, Ptacek LJ, Bates E (2012) An inwardly rectifying K+ Channel is required for patterning; Development. 2012 Oct; 139(19):3653-64.

Bates EA, Nikai T, Brennan KC, Fu YH, Charles AC, Basbaum A, Ptacek LJ, Ahn AH (2010) Sumatriptan alleviates mechanical and thermal allodynia in mice. Cephalalgia, Feb:30(2):170-8.

C. Voisine, H.Varma, N. Walker, Bates EA, Stockwell BR, Hart AC (2007) Identification of Potential Therapeutic Drugs for Huntington's Disease using Caenorhabditis elegans PLoS ONE. Jun 6;2(6):e504.

Bates EA, Jones A, Victor M, Shi Y, Hart AC (2006) Differential contributions of C. elegans histone deacetylases to Huntingtin polyglutamine toxicity; Journal of Neuroscience. Mar 8;26(10):2830-8.

Faber PW, Voisine C, King DC, Bates EA, Hart AC (2002) Glutamine/proline-rich PQE-1 proteins protect Caenorhabditis elegans neurons from huntingtin polyglutamine neurotoxicity. Proc Natl Acad Sci USA, Dec 24;99 (26):17131-6.

Simin K, Bates EA, Horner M, Letsou A (1998) Genetic analysis of Punt, a type II Dpp receptor that functions throughout the Drosophila melanogaster life cycle.  Genetics, 148: 801-813.

Bates Lab
University of Colorado Denver
RC1 North, 4th Floor, Room 4134
12800 E. 19th Avenue, Mailbox 8313
Aurora, CO  80045
Phone: 303-724-8303