Journal
CELL REPORTS
Volume 11, Issue 10, Pages 1651-1666Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.05.013
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Funding
- NIH [R01MH080434, R01MH078972, P30HD03352]
- International Rett Syndrome Foundation (IRSF) [2755]
- FRAXA
- University of Wisconsin-Madison Center for Stem Cells and Regenerative Medicine
- UW Hilldale fellowship for undergraduate research
- Epilepsy Foundation [310443]
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Fragile X mental retardation protein (FMRP) and its autosomal paralog FXR2P are selective neuronal RNA-binding proteins, and mice that lack either protein exhibit cognitive deficits. Although double-mutant mice display more severe learning deficits than single mutants, the molecular mechanism behind this remains unknown. In the present study, we discovered that FXR2P (also known as FXR2) is important for neuronal dendritic development. FMRP and FXR2P additively promote the maturation of new neurons by regulating a common target, the AMPA receptor GluA1, but they do so via distinct mechanisms: FXR2P binds and stabilizes GluA1 mRNA and enhances subsequent protein expression, whereas FMRP promotes GluA1 membrane delivery. Our findings unveil important roles for FXR2P and GluA1 in neuronal development, uncover a regulatory mechanism of GluA1, and reveal a functional convergence between fragile X proteins in neuronal development.
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