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Wnt Pathway Anomalies in Developing Amygdalae of Turner Syndrome-like Mice

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Abstract

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.

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Correspondence to Michael J. O’Neill.

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Raefski, A.S., Carone, B.R., Kaur, A. et al. Wnt Pathway Anomalies in Developing Amygdalae of Turner Syndrome-like Mice. J Mol Neurosci 32, 111–119 (2007). https://doi.org/10.1007/s12031-007-0022-7

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  • DOI: https://doi.org/10.1007/s12031-007-0022-7

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