Wnt Pathway Anomalies in Developing Amygdalae of Turner Syndrome-like Mice
pmid: 17873295
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.
- University of Connecticut United States
- University of Connecticut Health Center United States
Mice, Inbred C3H, X Chromosome, Reverse Transcriptase Polymerase Chain Reaction, Turner Syndrome, Amygdala, Mice, Inbred C57BL, Wnt Proteins, Disease Models, Animal, Mice, Pregnancy, Animals, Female, DNA Primers
Mice, Inbred C3H, X Chromosome, Reverse Transcriptase Polymerase Chain Reaction, Turner Syndrome, Amygdala, Mice, Inbred C57BL, Wnt Proteins, Disease Models, Animal, Mice, Pregnancy, Animals, Female, DNA Primers
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