Wnt pathway anomalies in developing amygdalae of Turner syndrome-like miceJournal of Molecular Neuroscience (2007)
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.
Citation InformationA. S. Raefski, Benjamin Carone, A. Kaur, W. Krueger, et al.. "Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice" Journal of Molecular Neuroscience Vol. 32 Iss. 2 (2007) p. 111 - 119
Available at: http://works.bepress.com/benjamin-carone/13/