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01.09.2009 | Article | Ausgabe 3/2009

Netherlands journal of psychology 3/2009

Genomic imprinting and communicative behaviour: Prader-Willi and Angelman syndrome

Zeitschrift:
Netherlands journal of psychology > Ausgabe 3/2009
Autor:
Harry Smit
Wichtige Hinweise
Department of Cognitive Neuroscience, Faculty of Psychology and Neuroscience, Maastricht UniversityCorrespondence to: Dr H.E. Smit, Department of Cognitive Neuroscience, Faculty of Psychology and Neuroscience, Maastricht University, PO Box 616, 6200 MD Maastricht, the Netherlands, Received 28 July 2008; revision accepted 20 June 2009.

Abstract

The kinship theory of genomic imprinting predicts that imprinted genes affect mother-child and child-child interactions. According to this theory paternally expressed genes will promote behaviours that increase costs of maternal investments and enable children to compete with siblings. Maternally expressed genes will promote behaviours that reduce the mother’s costs of child-rearing and enable children to engage in collaborative actions. Prader-Willi syndrome and Angelman syndrome are caused by the absence of expression of imprinted genes in 15q11-q13. Children with Prader-Willi syndrome lack the expression of paternally expressed genes; children with Angelman syndrome lack maternally expressed genes. The current paper discusses the role of imprinted genes in the development of communicative behaviours during the transition from breastfeeding to (consuming) solid food. Its focus is the possible role of imprinted genes in the development of empathy out of (reactive) crying, and in the development of behaviours necessary for joint action. Observed behavioural differences between children with Angelman and Prader-Willi syndrome, and data from mouse models on the effects of imprinted genes on brain development, are used to explore possible effects of imprinted genes. (Netherlands Journal of Psychology, 65, 78-88).

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