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Preso, A Novel PSD-95-Interacting FERM and PDZ Domain Protein That Regulates Dendritic Spine Morphogenesis

Authors
Lee, Hyun WooChoi, JeonghoonShin, HyewonKim, KaramYang, JinheeNa, MoonseokChoi, So YoenKang, Gil BuEom, Soo HyunKim, HyunKim, Eunjoon
Issue Date
31-12월-2008
Publisher
SOC NEUROSCIENCE
Keywords
PSD-95; WW; PDZ; FERM; actin; spine
Citation
JOURNAL OF NEUROSCIENCE, v.28, no.53, pp.14546 - 14556
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF NEUROSCIENCE
Volume
28
Number
53
Start Page
14546
End Page
14556
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/122188
DOI
10.1523/JNEUROSCI.3112-08.2008
ISSN
0270-6474
Abstract
PSD-95 is an abundant postsynaptic density (PSD) protein involved in the formation and regulation of excitatory synapses and dendritic spines, but the underlying mechanisms are not comprehensively understood. Here we report a novel PSD-95-interacting protein Preso that regulates spine morphogenesis. Preso is mainly expressed in the brain and contains WW( domain with two conserved Trp residues), PDZ (PSD-95/Dlg/ZO-1), FERM (4.1, ezrin, radixin, and moesin), and C-terminal PDZ-binding domains. These domains associate with actin filaments, the Rac1/Cdc42 guanine nucleotide exchange factor beta Pix, phosphatidylinositol-4,5-bisphosphate, and the postsynaptic scaffolding protein PSD-95, respectively. Preso overexpression increases the density of dendritic spines in a manner requiring WW, PDZ, FERM, and PDZ-binding domains. Conversely, knockdown or dominant-negative inhibition of Preso decreases spine density, excitatory synaptic transmission, and the spine level of filamentous actin. These results suggest that Preso positively regulates spine density through its interaction with the synaptic plasma membrane, actin filaments, PSD-95, and the beta Pix-based Rac1 signaling pathway.
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