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Author Notes:

Correspondence to James Q. Zheng: james.zheng@emory.edu

Author contributions: W. Lei performed most of the experiments and data analyses.

K.R. Myers helped with the brain slice work, and Y. Rui performed some of the imaging experiments.

S. Hladyshau and D. Tsygankov performed the curve fitting and computational modeling of the data.

J.Q. Zheng planned and oversaw the project.

W. Lei, K.R. Myers, and J.Q. Zheng wrote the manuscript.

The authors declare no competing financial interests.


Research Funding:

This project is supported in part by research grants from the National Institutes of Health to J.Q. Zheng (MH104632 and GM083889), a Ruth L. Kirschstein National Research Service Award Postdoctoral Fellowship to K.R. Myers (NS092342), and a National Institute of Neurological Disorders and Stroke core facilities grant (P30NS055077) to the Integrated Cellular Imaging Microscopy Core of Emory University.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • NECK

Phosphoinositide-dependent enrichment of actin monomers in dendritic spines regulates synapse development and plasticity


Journal Title:

Journal of Cell Biology


Volume 216, Number 8


, Pages 2551-2564

Type of Work:

Article | Final Publisher PDF


Dendritic spines are small postsynaptic compartments of excitatory synapses in the vertebrate brain that are modified during learning, aging, and neurological disorders. The formation and modification of dendritic spines depend on rapid assembly and dynamic remodeling of the actin cytoskeleton in this highly compartmentalized space, but the precise mechanisms remain to be fully elucidated. In this study, we report that spatiotemporal enrichment of actin monomers (G-actin) in dendritic spines regulates spine development and plasticity. We first show that dendritic spines contain a locally enriched pool of G-actin that can be regulated by synaptic activity. We further find that this G-actin pool functions in spine development and its modification during synaptic plasticity. Mechanistically, the relatively immobile G-actin pool in spines depends on the phosphoinositide PI(3,4,5)P 3 and involves the actin monomer-binding protein profilin. Together, our results have revealed a novel mechanism by which dynamic enrichment of G-actin in spines regulates the actin remodeling underlying synapse development and plasticity.

Copyright information:

© 2017 Lei et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (http://creativecommons.org/licenses/by-nc-sa/4.0/).

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