Rachel Wevrick

Rachel Wevrick


Medical Genetics
Medical Sciences Building
(780) 492-7908
(780) 492-1998 (fax)


Academic Degrees and Training

  • BSc: Queen's University
  • PhD: University of Toronto
  • Postdoctoral training: The Hospital for Sick Children, Toronto, Ont.
  • Postdoctoral training: Stanford University, Stanford, CA

Current Research Interests

Research Areas:

Genes and development, obesity, psychiatric disorders; mouse models for Prader-Willi syndrome; molecular basis of human genetic disorders.

Current research:

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.

If you are interested in a graduate student or postdoctoral position in my laboratory, please contact me at rwevrick@ualberta.ca, and include your cv.

Sources of Funding:

Projects in the Wevrick laboratory are funded by the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council, the Foundation for Prader-Willi Research, the Simons Foundation for Autism Research and the Women and Children's Health Research Institute. We also gratefully acknowledge funding from the Prader-Willi Syndrome Association of Alberta, the  Foundation for Prader-Willi Research (Canada) and One SMALL Step.

Donations in support of Prader-Willi Syndrome research in the Wevrick laboratory can be made by contacting the Office of Advancement at 1-888-799-9899, emailing giving@ualberta.ca, or by visiting "www.giving.ualberta.ca/ContactUs.aspx"

Selected Publications


1. A.A. Kamaludin, C. Smolarchuk, J.M. Bischof, R. Eggert, J.J. Greer, J. Ren, J.J. Lee, T. Yokota, F.B. Berry and R. Wevrick (2016) Muscle dysfunction caused by loss of Magel2 in a mouse model of Prader-Willi and Schaaf-Yang syndromes. Hum Molec Genet in press.

2. C. Luck, M.H. Vitaterna, and R. Wevrick. (2016) Dopamine pathway imbalance in mice lacking Magel2, a Prader-Willi syndrome candidate gene.  Behavioral Neuroscience 130:448-59 PMID: 27254754

3. J.M. Bischof, L.H.T. Van der Ploeg, W.F. Colmers and R. Wevrick. (2016) Magel2-null mice are hyper-responsive to setmelanotide, a melanocortin 4 receptor agonist.  Br. J. Pharm 173:2614-2621. PMID 27339818.

4. D.M. Arble, J.W. Pressler, J. Sorrell, R. Wevrick, D.A. Sandoval. (2016) Sleeve gastrectomy leads to weight loss in the Magel2 knockout mouse.  Surgery for Obesity and Related Diseases, S1550-7289, 30054-30055 PMID 27396546.

5. I. Pravdivyi, K. Ballanyi, W.F. Colmers, R. Wevrick (2015) Progressive postnatal decline in leptin sensitivity of arcuate hypothalmic neurons in the Magel2-null mouse model of Prader-Willi Syndrome. Hum. Molec. Genet. 24, 4276-4283.

6. X. Li, S. C. Hughes, R. Wevrick (2014) Evaluation of melanoma antigen gene (MAGE) expression in human cancers using The Cancer Genome Atlas. Cancer Genetics, 208:25-34.

7.  W.F. Colmers and R. Wevrick (2013) Leptin signaling defects in Prader-Willi syndrome-an orphan obesity syndrome no more. Rare Diseases 1, e24421.

8. R.E. Mercer, S.D. Michaelson, M.J.S. Chee, T.A. Atallah, R. Wevrick*, and W.F. Colmers*. (2013) Magel2 is required for leptin-mediated responses in POMC neurons in mice. PLoS Genetics 9: e1003207. (*joint senior authors).

9.  X. Li, R. Zhuo, S. Tiong, F. Di Cara, K. King-Jones, S. C. Hughes, S. D. Campbell, R. Wevrick (2013) The Smc5/Smc6/MAGE complex confers resistance to caffeine and genotoxic stress in Drosophila melanogaster. PLoS One, 8(3): e59866.

10. 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.

11. J. R. Bush and R. Wevrick. (2012) Loss of the Prader-Willi obesity syndrome protein necdin promotes adipogenesis. Gene, 497, 45-51.

12. 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.

13. J.R. Bush and R. Wevrick (2010) Loss of Necdin impairs myosin activation and delays cell polarization. Genesis: The Journal of Genetics and Development, 48:540-553.

14. R.E. Mercer and R. Wevrick (2009) Loss of Magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice. (2009) PLoS ONE. 4:e4291.

15. R.E. Mercer, E. M. Kwolek, J.M. Bischof, M. van Eede, R. M. Henkelman, and R. Wevrick. Abnormal behavior is associated with altered serotonin neurochemistry and regionally reduced brain volume in Magel2-null mice.(2009) Am. J. Med. Genetics 150B:1085-99


Jocelyn Bischof


Graduate Students

Vanessa Carias

Matthea Sanderson