ArticleMolecular biology of the cell2008
Arp2/3 complex is important for filopodia formation, growth cone motility, and neuritogenesis in neuronal cells.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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161 citing papers in PubMed, 291 citations in OpenAlex.
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- Vimentin filament transport and organization revealed by single-particle tracking and 3D FIB-SEM.The Journal of cell biology · 2025Article
- Hundreds of myosin 10s are pushed to the tips of filopodia and could cause traffic jams on actin.eLife · 2024Article
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- Hundreds of myosin 10s are pushed to the tips of filopodia and could cause traffic jams on actin.bioRxiv : the preprint server for biology · 2024Article
- Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models.Translational psychiatry · 2024Article
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- Understanding Actin Remodeling in Neuronal Cells Through Podosomes.Methods in molecular biology (Clifton, N.J.) · 2024Article
- ARP2/3 complex associates with peroxisomes to participate in pexophagy in plants.Nature plants · 2023Article
- Enabled primarily controls filopodial morphology, not actin organization, in the TSM1 growth cone inMolecular biology of the cell · 2023Article
- Gigaxonin is required for intermediate filament transport.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
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101 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
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Abstract
A role of Arp2/3 complex in lamellipodia is well established, whereas its roles in filopodia formation remain obscure. We addressed this question in neuronal cells, in which motility is heavily based on filopodia, and we found that Arp2/3 complex is involved in generation of both lamellipodia and filopodia in growth cones, and in neuritogenesis, the processes thought to occur largely in Arp2/3 complex-independent manner. Depletion of Arp2/3 complex in primary neurons and neuroblastoma cells by small interfering RNA significantly decreased the F-actin contents and inhibited lamellipodial protrusion and retrograde flow in growth cones, but also initiation and dynamics of filopodia. Using electron microscopy, immunochemistry, and gene expression, we demonstrated the presence of the Arp2/3 complex-dependent dendritic network of actin filaments in growth cones, and we showed that individual actin filaments in filopodia originated at Arp2/3 complex-dependent branch points in lamellipodia, thus providing a mechanistic explanation of Arp2/3 complex functions during filopodia formation. Additionally, Arp2/3 complex depletion led to formation of multiple neurites, erratic pattern of neurite extension, and excessive formation of stress fibers and focal adhesions. Consistent with this phenotype, RhoA activity was increased in Arp2/3 complex-depleted cells, indicating that besides nucleating actin filaments, Arp2/3 complex may influence cell motility by altering Rho GTPase signaling.
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