Journal
CURRENT BIOLOGY
Volume 20, Issue 2, Pages 103-115Publisher
CELL PRESS
DOI: 10.1016/j.cub.2009.12.030
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Funding
- Czech Science Foundation [GACR303/08/1591]
- Academy of Sciences of the Czech Republic [AV0Z50520514]
- Ministry of Education, Youth and Sports of the Czech Republic [VZ MSM 0021620820]
- Telethon Italy [GGP05236A, GGP06208]
- Compagnia di San Paolo
- Spanish Ministerio de Educacion y Ciencia [EX2006-0294]
- Agence Nationale pour la Recherche [ANR-05-Neuro-040-01, ANR-06-Neuro-003-02]
- Fondation Jerome Lejeune
- Inserm
- Fondazione Cariplo [2006-0779, 2008-2318]
- Compagnia di San Paolo [2005.1964]
- RSTL-CNR
- PRIN
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Background: Interleukin-1 receptor accessory protein-like 1 (IL1RAPL1) gene mutations are associated with cognitive impairment ranging from nonsyndromic X-linked mental retardation to autism. IL1RAPL1 belongs to a novel family of Toll/IL-1 receptors, whose expression in the brain is upregulated by neuronal activity. Currently, very little is known about the function of this protein. We previously showed that IL1RAPL1 interacts with the neuronal calcium sensor NCS-1 and that it regulates voltage-gated calcium channel activity in PC12 cells. Results: Here we show that IL1RAPL1 is present in dendritic spine where it interacts with PSD-95, a major component of excitatory postsynaptic compartment. Using gain- and loss-of-function experiments in neurons, we demonstrated that IL1RAPL1 regulates the synaptic localization of PSD-95 by controlling c-Jun terminal kinase (JNK) activity and PSD-95 phosphorylation. Mice carrying a null mutation of the mouse Il1rapl1 gene show a reduction of both dendritic spine density and excitatory synapses in the CA1 region of the hippocampus. These structural abnormalities are associated with specific deficits in hippocampal long-term synaptic plasticity.
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