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J Cell Biol. 2016 Feb 15;212(4):449-63. doi: 10.1083/jcb.201509023.

Neuroligin 1 regulates spines and synaptic plasticity via LIMK1/cofilin-mediated actin reorganization.

Author information

1
The Key Laboratory of Developmental Genes and Human Disease, Jiangsu Co-innovation Center of Neuroregeneration, Southeast University, Nanjing 210096, China.
2
The Key Laboratory of Developmental Genes and Human Disease, Jiangsu Co-innovation Center of Neuroregeneration, Southeast University, Nanjing 210096, China Institute of Life Sciences, The Collaborative Innovation Center for Brain Science, Southeast University, Nanjing 210096, China.
3
Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario M5S 1A8, Canada.
4
Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, DC 20007.
5
Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario M5S 1A8, Canada zhengping.jia@sickkids.ca wei.xie@seu.edu.cn.
6
The Key Laboratory of Developmental Genes and Human Disease, Jiangsu Co-innovation Center of Neuroregeneration, Southeast University, Nanjing 210096, China Institute of Life Sciences, The Collaborative Innovation Center for Brain Science, Southeast University, Nanjing 210096, China zhengping.jia@sickkids.ca wei.xie@seu.edu.cn.

Abstract

Neuroligin (NLG) 1 is important for synapse development and function, but the underlying mechanisms remain unclear. It is known that at least some aspects of NLG1 function are independent of the presynaptic neurexin, suggesting that the C-terminal domain (CTD) of NLG1 may be sufficient for synaptic regulation. In addition, NLG1 is subjected to activity-dependent proteolytic cleavage, generating a cytosolic CTD fragment, but the significance of this process remains unknown. In this study, we show that the CTD of NLG1 is sufficient to (a) enhance spine and synapse number, (b) modulate synaptic plasticity, and (c) exert these effects via its interaction with spine-associated Rap guanosine triphosphatase-activating protein and subsequent activation of LIM-domain protein kinase 1/cofilin-mediated actin reorganization. Our results provide a novel postsynaptic mechanism by which NLG1 regulates synapse development and function.

PMID:
26880202
PMCID:
PMC4754719
DOI:
10.1083/jcb.201509023
[Indexed for MEDLINE]
Free PMC Article

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