EVL and MIM/MTSS1 regulate actin cytoskeletal remodeling to promote dendritic filopodia in neurons

Sara S. Parker, Kenneth Tran Ly, Adam D. Grant, Jillian Sweetland, Ashley M. Wang, James D. Parker, Mackenzie R. Roman, Kathylynn Saboda, Denise J. Roe, Megha Padi, Charles W. Wolgemuth, Paul Langlais, Ghassan Mouneimne

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Dendritic spines are the postsynaptic compartment of a neuronal synapse and are critical for synaptic connectivity and plasticity. A developmental precursor to dendritic spines, dendritic filopodia (DF), facilitate synapse formation by sampling the environment for suitable axon partners during neurodevelopment and learning. Despite the significance of the actin cytoskeleton in driving these dynamic protrusions, the actin elongation factors involved are not well characterized. We identified the Ena/VASP protein EVL as uniquely required for the morphogenesis and dynamics of DF. Using a combination of genetic and optogenetic manipulations, we demonstrated that EVL promotes protrusive motility through membrane-direct actin polymerization at DF tips. EVL forms a complex at nascent protrusions and DF tips with MIM/MTSS1, an I-BAR protein important for the initiation of DF. We proposed a model in which EVL cooperates with MIM to coalesce and elongate branched actin filaments, establishing the dynamic lamellipodia-like architecture of DF.

Original languageEnglish (US)
JournalThe Journal of cell biology
Volume222
Issue number5
DOIs
StatePublished - May 1 2023

ASJC Scopus subject areas

  • Cell Biology

Fingerprint

Dive into the research topics of 'EVL and MIM/MTSS1 regulate actin cytoskeletal remodeling to promote dendritic filopodia in neurons'. Together they form a unique fingerprint.

Cite this