Wnt pathway anomalies in developing amygdalae of Turner Syndrome-like mice

Adam S. Raefski, Benjamin R. Carone, Anupinder Kaur, Winfried Krueger, Michael J. O'Neill

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Certain neurobehavioral deficiencies associated with Turner Syndrome have been attributed to brain volumetric abnormalities, particularly of the amygdala. Haplo-insufficiency of a non-dosage compensated gene or genes on the X chromosome has been hypothesized to be the cause of the neuroanatomical defect. We examined gene expression levels of 6,628 genes in developing amygdalae of late-stage embryos of a mouse model for Turner Syndrome. In total, 161 genes show significant differences in expression level between TS and normal female amygdala. In silico pathway analysis of both X-linked and autosomal mis-regulated genes suggests that modulation of Wnt signaling is a critical factor in the normal growth and development of the amygdala.

Original languageEnglish (US)
Pages (from-to)111-119
Number of pages9
JournalJournal of Molecular Neuroscience
Issue number2
StatePublished - Jun 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience


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