A novel mouse model of Prader-Willi Syndrome including the deletion of both Necdin and Magel2 genes

Prader-Willi syndrome (PWS) is a multigenic disorder caused by the loss of seven contiguous paternally expressed genes. Mouse models with inactivation of all PWS genes display 100% lethality within the first postnatal week and have not helped understand the postnatal pathophysiology of this syndrome. Knockout (KO) models for each candidate gene were also generated, but they lack the functional interactions and possible compensatory functions between PWS-related genes. Here, we generated a novel double KO mouse model to explore the effect of a combined deletion of Magel2 and Necdin. Mice were maintained under standard animal housing conditions, with free access to food and water,, and in standard 12-h light/12-h dark cycles (LD). C57BL/6J mice (WT) and double ko mice (MADIN) were sacrificed either six hour after light on (the DAY group) or 18 hours after light on (the NIGHT group) and were processed for total RNA sequencing