Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice.
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.
Raefski
Adam S
AS
Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA.
Carone
Benjamin R
BR
Kaur
Anupinder
A
Krueger
Winfried
W
O'Neill
Michael J
MJ
D000679:Amygdala / Q000254:growth & development / Q000503:physiopathology*; D000818:Animals; D017931:DNA Primers; D004195:Disease Models, Animal; D005260:Female; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D011247:Pregnancy; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014424:Turner Syndrome / Q000196:embryology / Q000235:genetics*; D051153:Wnt Proteins / Q000235:genetics*; D014960:X Chromosome
D017931:DNA Primers; D051153:Wnt Proteins