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Paradoxical leanness in the imprinting-centre deletion mouse model for Prader–Willi syndrome

David M Golding

David M Golding School of Biosciences, Cardiff University, Cardiff, UK

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Daniel J Rees

Daniel J Rees Institute of Life Sciences, College of Medicine, Swansea University, Swansea, UK

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Jennifer R Davies

Jennifer R Davies Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Dinko Relkovic

Dinko Relkovic Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Hannah V Furby

Hannah V Furby Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Irina A Guschina

Irina A Guschina School of Biosciences, Cardiff University, Cardiff, UK

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Anna L Hopkins

Anna L Hopkins School of Biosciences, Cardiff University, Cardiff, UK

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Jeffrey S Davies

Jeffrey S Davies Institute of Life Sciences, College of Medicine, Swansea University, Swansea, UK

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James L Resnick

James L Resnick Center for Mammalian Genetics, University of Florida, College of Medicine, Gainesville, Florida, USA

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Anthony R Isles

Anthony R Isles Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Timothy Wells

Timothy Wells School of Biosciences, Cardiff University, Cardiff, UK

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Introduction Prader–Willi syndrome (PWS) is caused by a lack of paternal gene expression from the 15q11–q13 imprinting cluster and results from large chromosomal deletions, chromosome 15 maternal uniparental disomy or imprinting-centre (IC