PMID:15380068

Citation	Israely, I, Costa, RM, Xie, CW, Silva, AJ, Kosik, KS and Liu, X (2004) Deletion of the neuron-specific protein delta-catenin leads to severe cognitive and synaptic dysfunction. Curr. Biol. 14:1657-63
Abstract	Delta-catenin (delta-catenin) is a neuron-specific catenin, which has been implicated in adhesion and dendritic branching. Moreover, deletions of delta-catenin correlate with the severity of mental retardation in Cri-du-Chat syndrome (CDCS), which may account for 1% of all mentally retarded individuals. Interestingly, delta-catenin was first identified through its interaction with Presenilin-1 (PS1), the molecule most frequently mutated in familial Alzheimer's Disease (FAD). We investigated whether deletion of delta-catenin would be sufficient to cause cognitive dysfunction by generating mice with a targeted mutation of the delta-catenin gene (delta-cat(-/-)). We observed that delta-cat(-/-) animals are viable and have severe impairments in cognitive function. Furthermore, mutant mice display a range of abnormalities in hippocampal short-term and long-term synaptic plasticity. Also, N-cadherin and PSD-95, two proteins that interact with delta-catenin, are significantly reduced in mutant mice. These deficits are severe but specific because delta-cat(-/-) mice display a variety of normal behaviors, exhibit normal baseline synaptic transmission, and have normal levels of the synaptic adherens proteins E-cadherin and beta-catenin. These data reveal a critical role for delta-catenin in brain function and may have important implications for understanding mental retardation syndromes such as Cri-du-Chat and neurodegenerative disorders, such as Alzheimer's disease, that are characterized by cognitive decline.
Links	PubMed Online version:10.1016/j.cub.2004.08.065
Keywords	Analysis of Variance; Animals; Armadillo Domain Proteins; Cadherins/metabolism; Catenins; Cell Adhesion Molecules; Cognition Disorders/etiology; Conditioning (Psychology)/physiology; Cytoskeletal Proteins/deficiency; Cytoskeletal Proteins/genetics; Electrophysiology; Fear/physiology; Guanylate Kinase; Hippocampus/physiopathology; Immunoprecipitation; Intracellular Signaling Peptides and Proteins; Maze Learning/physiology; Membrane Proteins; Mice; Mice, Mutant Strains; Mutation/genetics; Nerve Tissue Proteins/metabolism; Neurodegenerative Diseases/etiology; Neuronal Plasticity/physiology; Neurons/metabolism; Phosphoproteins; Psychomotor Performance/physiology; Synapses/genetics; Synapses/metabolism
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