Durak, Omerde Anda, Froylan CalderonSingh, Karun K.Leussis, Melanie P.Petryshen, Tracey L.Sklar, PamelaTsai, Li-Huei2015-10-012014Durak, Omer, Froylan Calderon de Anda, Karun K. Singh, Melanie P. Leussis, Tracey L. Petryshen, Pamela Sklar, and Li-Huei Tsai. 2014. “Ankyrin-G Regulates Neurogenesis and Wnt Signaling by Altering the Subcellular Localization of β-catenin.” Molecular psychiatry 20 (3): 388-397. doi:10.1038/mp.2014.42. http://dx.doi.org/10.1038/mp.2014.42.1359-4184http://nrs.harvard.edu/urn-3:HUL.InstRepos:22857060Ankyrin-G is a scaffolding protein required for the formation of the axon initial segment in neurons. Recent genome-wide association studies and whole-exome sequencing have identified ANK3, the gene coding for ankyrin-G, to be a risk gene for multiple neuropsychiatric disorders such as bipolar disorder (BD), schizophrenia, and autism spectrum disorder (ASD). Here, we describe a novel role for ankyrin-G in neural progenitor proliferation in the developing cortex. We found that ankyrin-G regulates canonical Wnt signaling by altering the subcellular localization and availability of β-catenin in proliferating cells. Ankyrin-G loss-of-function increases β-catenin levels in the nucleus, thereby promoting neural progenitor proliferation. Importantly, abnormalities in proliferation can be rescued by reducing Wnt pathway signaling. Together, these results suggest that ankyrin-G is required for proper brain development.en-USANK3Ankyrin-GWntNeurogenesisNeuropsychiatric DisordersJournal Article2015-10-0110.1038/mp.2014.42