Role of MAGEL2 in Excitatory Synapse Function

Funding Summary

Dr. Atasoy and his team have recently discovered that the protein Magel2 is important in allowing oxytocin neurons in the brain to communicate normally. These neurons are involved in social behavior, cognition and infant feeding. This funded project will study a mouse model of PWS that is lacking Magel2, to understand how loss of Magel2 impacts communication of these neurons, and how brain circuits change when Magel2 is missing.

This project was funded by FPWR-Canada.


Watch the full webinar describing all 9 research projects funded in this grant cycle here


Lay Abstract

Prader Willi Syndrome (PWS) is a debilitating genetic disorder effecting brain function and behavior. Although the impaired genes have long been known, how their deletion cause behavioral problems that are seen in PWS patients has not been understood. The lack of knowledge on the cellular function of these genes makes it difficult to understand the nature of impairments and thus limiting the development of therapeutic strategies. Magel2 is one of the PWS inactivated genes that is highly expressed in the brain. We have recently discovered that Magel2 is required for normal communication between a subset of neurons, marked by presence of oxytocin peptide, that is known to be involved in social behavior and infant feeding. Our objective in this proposal is to gain further insight into the role of Magel2 function in neuronal communication. We will test whether other Magel2 expressing neurons also have similar communication problems. To address this, we will focus on a region called amygdala, a brain region known to be involved in PWS impaired phenotypes such as social learning and aggression. Furthermore, Magel2 is expressed in high levels in this region. Using single-cell gene expression analysis, we will first characterize specifically which amygdala cell types express Magel2. We will then examine communication between those brain cells using special techniques like single neuron activity recording, to understand how defective Magel2 expression impairs amygdala circuit function. Knowing how and which brain circuits affected in Magel2 deficiency, will enable informed strategies for mitigating the effects of their dysfunction.

Research Outcomes: Public Summary

Our findings suggest that, overall medial amygdala neuron functional properties are not altered in Magel2 deficient mice.

Funded Year:


Awarded to:

Deniz Atasoy, Ph.D.




University of Iowa


Deniz Atasoy, Ph.D.

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