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Investigation of the Prader-Willi syndrome protein MAGEL2 in the regulation of Forkhead box transcription factor FOXO1 Open Access


Other title
nucleocytoplasmic shuttling
Forkhead box transcription factor
Prader-Willi syndrome
melanoma-associated antigen
Type of item
Degree grantor
University of Alberta
Author or creator
Devos, Julia J
Supervisor and department
Wevrick, Rachel (Medical Genetics)
Examining committee member and department
Berry, Fred (Surgery/Medical Genetics)
Wevrick, Rachel (Medical Genetics)
Haqq, Andrea (Pediatrics)
McDermid, Heather (Biological Sciences/Medical Genetics)
Medical Sciences-Medical Genetics

Date accepted
Graduation date
Master of Science
Degree level
Prader-Willi syndrome (PWS), a genetic disorder resulting from the loss of expression of multiple genes including MAGEL2, is characterized by hyperphagia and childhood-onset obesity. These symptoms point to dysfunction in the regulation of energy homeostasis. Magel2 is highly expressed in the hypothalamus, the body’s main regulator of energy balance. As the Forkhead box transcription factor FOXO1 functions in the hypothalamus to regulate food intake and body weight, I hypothesized that MAGEL2 may be involved in energy homeostasis by regulating FOXO1. Although no interaction was detected between these two proteins, I determined that MAGEL2 alters FOXO1 subcellular localization in a manner dependent upon post-translational modifications of FOXO1. Expression of MAGEL2 increases cytoplasmic localization of acetylated and phosphorylated FOXO1 and increases nuclear localization of deaceteylated FOXO1 in immunofluorescence experiments. The loss of MAGEL2 expression in PWS may impair proper FOXO1 regulation, reducing the ability of the hypothalamus to maintain energy homeostasis.
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Citation for previous publication
Devos, J., Weselake, S.V., and Wevrick, R. (2011). Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells. J. Circadian Rhythms 9, 12.

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