Journal
CELL REPORTS
Volume 31, Issue 2, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.03.059
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Funding
- NINDS [R01 NS34661, R01 NS099099]
- Simons Foundation [630332]
- NIMH [R01MH100292, R01MH106507]
- Nina Ireland
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Tbr1 is a high-confidence autism spectrum disorder (ASD) gene encoding a transcription factor with distinct pre- and postnatal functions. Postnatally, Tbr1 conditional knockout (CKO) mutants and constitutive heterozygotes have immature dendritic spines and reduced synaptic density. Tbr1 regulates expression of several genes that underlie synaptic defects, including a kinesin (Kif1a) and a WNT-signaling ligand (Wnt7b). Furthermore, Tbr1 mutant corticothalamic neurons have reduced thalamic axonal arborization. LiCl and a GSK3 beta inhibitor, two WNT-signaling agonists, robustly rescue the dendritic spines and the synaptic and axonal defects, suggesting that this could have relevance for therapeutic approaches in some forms of ASD.
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