Rachel Wevrick, PhD
Office: 8-16A Medical Sciences Building
Mail: University of Alberta, Edmonton AB T6G 2H7
Phone: 780-492-7908 (Office)
Professor, Department of Medical Genetics
AHFMR Senior Scholar
Member, Centre for Neuroscience
Member, CIHR Strategic Training Program in Maternal, Fetal, and Newborn Health
Member, Canadian Obesity Network
Genes and development, obesity, psychiatric disorders; mouse models for Prader-Willi syndrome; molecular basis of human genetic disorders.
Research in the Wevrick laboratory focuses on genetic disorders that affect human development. We have specific interests in pediatric obesity, developmental delay, and also study developmental aspects of gene regulation. We identified genes that are inactivated in Prader-Willi syndrome, a sporadic chromosomal disorder that causes neonatal hypotonia, developmental delay, compulsive overeating leading to obesity, and abnormalities of sleep and respiration. We are currently studying the roles of these genes in the normal development of the nervous, muscular, and endocrine systems. Two genes, necdin and MAGEL2, have specific roles in growth and differentiation. We are using mouse models to evaluate the normal roles of these proteins and the effect of their loss in Prader-Willi syndrome. This work is funded by CIHR, NSERC, and the Foundation for Prader-Willi Research.
Other Activities and Affiliations
- Academic Lead, Research Education, Women and Children's Health Research Institute
- Member, Alberta Diabetes Institute
- Member, Centre for Neuroscience
- Member, Scientific Advisory Board, Prader-Willi Syndrome Association (USA)
- Member, Scientific Board of Directors, Foundation for Prader-Willi Research (USA)
Degrees: B.Sc (Hon), Queen's University,
Ph.D, University of Toronto
Postdoctoral: Hospital for Sick Children (Toronto), Stanford University
Rachel Wevrick co-discovered many of the genes inactivated in Prader-Willi syndrome, including Necdin, MAGEL2, and IPW. Her research focuses on the genetic basis of developmental delay and obesity, using tools in molecular and cellular biology and mouse models to investigate the gene and protein function, specializing in the development of the nervous, muscle, and endocrine systems.
1. R.E. Mercer, S.D. Michaelson, M.J.S. Chee, T.A. Atallah, R. Wevrick*, and W.F. Colmers*. Magel2 is required for leptin-mediated responses in POMC neurons in mice. PLoS Genetics, in press. (*joint senior authors).
2. R. E. Mercer and R. Wevrick (2012). Energy homeostasis in Prader-Willi Syndrome: how clinical research informs studies of animal models of genetic obesity. Am. J. Med. Genetics A, 158A: 966-9668.
3. J. R. Bush and R. Wevrick. (2012) Loss of the Prader-Willi obesity syndrome protein necdin promotes adipogenesis. Gene, 497, 45-51.
4. J. Devos, S.V. Weselake, and R. Wevrick. (2012) Magel2, a Prader-Willi Syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells. J. Circadian Rhythms, 9:12.
5. T. Asai, Y. Liu, S. Di Giandomenico, N. Bae, D. Ndiaye-Lobry, A. Deblasio, S. Menendez, Y. Antipin, B. Reva, R. Wevrick, and S. D. Nimer (2012). Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells. Blood, 120:1601-1612.
6. A. A. Tennese and R. Wevrick. (2011) Impaired hypothalamic regulation of endocrine function and delayed counter-regulatory response to hypoglycemia in Magel2-null mice. Endocrinology 152, 967-978.
7. J. R. Bush and R. Wevrick (2010) Impaired myosin activation and cellular polarization contribute to defective neuronal and muscle development in a necdin-deficient mouse model of Prader-Willi syndrome. genesis: The Journal of Genetics and Development, 48:540-553.
8. N.L.G. Miller, R. Wevrick, P.L. Mellon (2009). Necdin, a Prader-Willi syndrome candidate gene, regulates the development of gonadotropin-releasing hormone neurons. Human Molec. Genetics 18:248-260. Evaluated by Faculty of 1000
9. R. E. Mercer and R. Wevrick (2009). Loss of Magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice. PLoS ONE 4(1): e4291.
10. R. E. Mercer, E. M. Kwolek, J.M. Bischof, M. van Eede, R. M. Henkelman, and R. Wevrick (2009). Regionally reduced brain volume, altered serotonin neurochemistry, and abnormal behavior in mice null for the circadian rhythm output gene Magel2. Am. J. Med. Genetics B 150B: 1085–1099.
11. A. A. Tennese, C. B. Gee, and R. Wevrick. (2008). Loss of the Prader-Willi syndrome protein necdin causes defective migration, axonal outgrowth, and survival of embryonic sympathetic neurons. Developmental Dynamics 20:1935-1943. Evaluated by Faculty of 1000
12. J.R. Bush and R. Wevrick (2008). The Prader-Willi syndrome protein necdin interacts with the E1A-like inhibitor of differentiation EID-1 and promotes myoblast differentiation. Differentiation 76:994-1005.
13. S. Koslov, J. W. Bogenpohl, M. P. Howell, R. Wevrick, S. Panda, J.B. Hogenesch, L. J. Muglia, R. Van Gelder, E. D. Herzog, C. L. Stewart (2007). The imprinted gene Magel2 regulates normal circadian output. Nature Genetics 39, 1266 - 1272.
14. J. M. Bischof, C. L. Stewart, and R. Wevrick (2007). Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi Syndrome. Human Molec. Genetics 16: 2713-2719.
Website Links of Interest
Dept. of Medical Genetics