title: Activity-dependent modulation of the interaction between CaMKIIα and Abi1 and its involvement in spine maturation.
abstract: Remodeling of dendritic spines through regulation of actin dynamics is a key event in activity-dependent structural plasticity. However, the molecular mechanism underlying this process is poorly understood. Here, we show that activity-dependent modulation of Abl interactor 1-Ca(2+)/calmodulin-dependent kinase IIα (Abi1-CaMKIIα) interaction, and thereby their activity, is important for regulation of spine morphology in cultured rat hippocampal neurons. Abi1 interacts with CaMKIIα at resting conditions through Abi1's tSNARE (target membrane-associated SNARE), which harbors striking homology with CaMKIIα regulatory domain. The interaction of the two proteins, Abi1 and CaMKIIα, results in their simultaneous inhibition, inhibition of CaMKIIα activity, and also inhibition of Abi1-dependent Rac activation. Their functional impediment is released when they dissociate from each other by calmodulin binding through glutamate receptor activation. Before dissociation, Abi1 is phosphorylated by CaMKIIα at serine 88, which may involve in regulation of Rac activation and spine maturation. Our results suggest that modulation of the interaction between Abi1 and CaMKIIα, through the glutamate receptor pathway, may be a molecular mechanism underlying activity-regulated structural plasticity in rat hippocamapal neurons.
authors.affiliation: School of Biological Sciences, Seoul National University, Seoul 151-747, South Korea.
authors.forename: Esther
authors.initials: E
authors.lastname: Park
authors.forename: Susan
authors.initials: S
authors.lastname: Chi
authors.forename: Dongeun
authors.initials: D
authors.lastname: Park
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000493:pharmacokinetics; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002122:Calcium Chloride / Q000494:pharmacology; D061207:Calcium Ionophores / Q000494:pharmacology; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000235:genetics / Q000378:metabolism*; D020134:Catalytic Domain / Q000502:physiology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D049229:Dendritic Spines / Q000502:physiology*; D004622:Embryo, Mammalian; D018683:Excitatory Amino Acid Agents / Q000494:pharmacology; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D018698:Glutamic Acid / Q000494:pharmacology; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology; D006801:Humans; D047468:Immunoprecipitation; D007456:Iodine Isotopes / Q000493:pharmacokinetics; D015759:Ionomycin / Q000494:pharmacology; D016202:N-Methylaspartate / Q000494:pharmacology; D009474:Neurons / Q000648:ultrastructure; D010766:Phosphorylation; D011485:Protein Binding / Q000187:drug effects / Q000235:genetics; D050765:Qa-SNARE Proteins / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D050600:SNARE Proteins / Q000378:metabolism; D012694:Serine / Q000378:metabolism; D013569:Synapses / Q000378:metabolism; D014162:Transfection; D050598:Vesicular Glutamate Transport Protein 1 / Q000378:metabolism
chemical_list: C554931:Abi1 protein, rat; D048868:Adaptor Proteins, Signal Transducing; D061207:Calcium Ionophores; D018683:Excitatory Amino Acid Agents; D051272:Glucose Transporter Type 1; D007456:Iodine Isotopes; D050765:Qa-SNARE Proteins; D034741:RNA, Small Interfering; D050600:SNARE Proteins; C493466:Slc17a7 protein, rat; C495679:Slc2a1 protein, rat; D050598:Vesicular Glutamate Transport Protein 1; D049452:Green Fluorescent Proteins; D018698:Glutamic Acid; D012694:Serine; D015759:Ionomycin; D016202:N-Methylaspartate; D000255:Adenosine Triphosphate; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D002122:Calcium Chloride; D002118:Calcium