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Global neurodevelopmental delay is a prominent characteristic of individuals withPrader-Willi syndrome (PWS). The neuromolecular bases for these delays are unknown. Weidentified neuroanatomical changes in the brains of mice deficient for a gene in theminimal critical deletion region for PWS ( Snord116 p−/m+  ). InSnord116 p−/m+   mice, reduced primary forebrain neuron cellbody size is apparent in embryonic day 15.5 fetuses, and persists until postnatal day 30in cerebellar Purkinje neurons.  Snord116  is a snoRNA gene cluster ofunknown function that can localize to the nucleolus. In cerebellar Purkinje neurons frompostnatal day 30  Snord116 p−/m+   mice the reduction in neuronalcell body size was associated with decreased neuronal nucleolar size. We also identifieddevelopmental changes in the endocrine pancreas ofSnord116 p−/m+   animals that persist into adulthood. Micelacking  Snord116  have smaller pancreatic islets; within the islet thepercentage of δ-cells is increased, while the percentage of α-cells is reduced. The α-cellmarkers,  Sst  and  Hhex,  are upregulated inSnord116 p−/m+   isolated islets while  Ins1, Ins2,Pdx1, Nkx6-1,  and  Pax6  are downregulated. There is a 3-foldincrease in the percentage of polyhormonal cells in the neonatal pancreata ofSnord116 p−/m+   mice, due primarily to an increase in cellsco-positive with somatostatin.  Snord116  may play a role in islet celllineage specification. The  Snord116  gene cluster is important fordevelopmental processes in the brain as well as the endocrine pancreas.

human molecular genetics

Loss of the imprinted, non-coding  Snord116  gene cluster in           the interval deleted in the Prader Willi syndrome results in murine neuronal and endocrine           pancreatic developmental phenotypes