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MAGED1 ,  NECDIN  and  MAGEL2  are members of the  MAGE  gene family. The latter two of these genes have been involved in Prader–Willi syndrome (PWS), which includes hyperphagia, repetitive and compulsive behaviors, and cognitive impairment. Here, we show that  Maged1 -deficient mice develop progressive obesity associated with hyperphagia and reduced motor activity. Loss of  Maged1  also results in a complex behavioral syndrome that includes reduced social interactions and memory, deficient sexual behavior, as well as increased anxiety and self-grooming. Oxytocin (OT), which is produced in the hypothalamus, can act as a neurotransmitter that reduces anxiety, promotes social behaviors and regulates food intake. Growing evidences indicate that OT is involved in autism. We found that  Maged1  mutants showed a severe reduction in the levels of mature OT, but not of its precursors, in the hypothalamus. Moreover, the administration of OT rescued the deficit in social memory of these mice. We conclude that Maged1 is required for OT processing or stability. A decrease in mature OT levels in  Maged1  mutants affects social interactions and possibly other behavioral processes. Our observations suggest that, in human,  MAGED1  could play a role in autism or cause a neurodevelopmental condition that is reminiscent of the PWS.

human molecular genetics

Loss of  Maged1  results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus