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Open Access Green as soon as Postprint is submitted to ZB.
MIM-induced membrane bending promotes dendritic spine initiation.
Dev. Cell 33, 644-659 (2015)
Proper morphogenesis of neuronal dendritic spines is essential for the formation of functional synaptic networks. However, it is not known how spines are initiated. Here, we identify the inverse-BAR (I-BAR) protein MIM/MTSS1 as a nucleator of dendritic spines. MIM accumulated to future spine initiation sites in a PIP2-dependent manner and deformed the plasma membrane outward into a proto-protrusion via its I-BAR domain. Unexpectedly, the initial protrusion formation did not involve actin polymerization. However, PIP2-dependent activation of Arp2/3-mediated actin assembly was required for protrusion elongation. Overexpression of MIM increased the density of dendritic protrusions and suppressed spine maturation. In contrast, MIM deficiency led to decreased density of dendritic protrusions and larger spine heads. Moreover, MIM-deficient mice displayed altered glutamatergic synaptic transmission and compatible behavioral defects. Collectively, our data identify an important morphogenetic pathway, which initiates spine protrusions by coupling phosphoinositide signaling, direct membrane bending, and actin assembly to ensure proper synaptogenesis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Missing-in-metastasis; F-bar Domain; Actin Cytoskeleton; Plasma-membrane; Irsp53; Morphogenesis; Plasticity; Proteins; Dynamics; Shape
ISSN (print) / ISBN
1534-5807
e-ISSN
1878-1551
Journal
Developmental Cell
Quellenangaben
Volume: 33,
Issue: 6,
Pages: 644-659
Publisher
Elsevier
Publishing Place
Cambridge
Non-patent literature
Publications
Reviewing status
Peer reviewed