ArticleNature cell biology2009
Myosin IIIa boosts elongation of stereocilia by transporting espin 1 to the plus ends of actin filaments.
Article in Nature cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 151 citations in OpenAlex.
- Characterization of a novel MYO3A missense mutation associated with a dominant form of late onset hearing loss.Scientific reports · 2018Trial
- Exploring phosphoregulation of MYO3A using quantitative fluorescence image analysis in COS7 cells.microPublication biology · 2026Article
- Single-molecule fluorescence microscopy reveals regulatory mechanisms of MYO7A-driven cargo transport in stereocilia of live inner ear hair cells.Nature communications · 2025Article
- Myosin-based nucleation of actin filaments contributes to stereocilia development critical for hearing.Nature communications · 2025Article
- The Prevalence and Clinical Characteristics ofGenes · 2025Article
- Pathophysiology of human hearing loss associated with variants in myosins.Frontiers in physiology · 2024Review
- Article
- The actin cytoskeleton in hair bundle development and hearing loss.Hearing research · 2023Review
- Article
- Actin Bundles Dynamics and Architecture.Biomolecules · 2023Review
- Liquid-liquid phase separation in hair cell stereocilia development and maintenance.Computational and structural biotechnology journal · 2023Review
- Selective binding and transport of protocadherin 15 isoforms by stereocilia unconventional myosins in a heterologous expression system.Scientific reports · 2022Article
- Deafness-related protein PDZD7 forms complex with the C-terminal tail of FCHSD2.The Biochemical journal · 2022Article
- High-resolution immunofluorescence imaging of mouse cochlear hair bundles.STAR protocols · 2022Article
- Collapsin Response Mediator Protein 1 (CRMP1) Is Required for High-Frequency Hearing.The American journal of pathology · 2022Article
- Human deafness-associated variants alter the dynamics of key molecules in hair cell stereocilia F-actin cores.Human genetics · 2022Review
- Deafness mutation in the MYO3A motor domain impairs actin protrusion elongation mechanism.Molecular biology of the cell · 2022Article
- Grxcr1 regulates hair bundle morphogenesis and is required for normal mechanoelectrical transduction in mouse cochlear hair cells.PloS one · 2022Article
- Studies of functional properties of espin 1: Its interaction to actin filaments.Frontiers in cell and developmental biology · 2022Article
- E3 ubiquitin ligase ASB17 is required for spermiation in mice.Translational andrology and urology · 2021Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Two proteins implicated in inherited deafness, myosin IIIa, a plus-end-directed motor, and espin, an actin-bundling protein containing the actin-monomer-binding motif WH2, have been shown to influence the length of mechanosensory stereocilia. Here we report that espin 1, an ankyrin repeat-containing isoform of espin, colocalizes with myosin IIIa at stereocilia tips and interacts with a unique conserved domain of myosin IIIa. We show that combined overexpression of these proteins causes greater elongation of stereocilia, compared with overexpression of either myosin IIIa alone or espin 1 alone. When these two proteins were co-expressed in the fibroblast-like COS-7 cell line they induced a tenfold elongation of filopodia. This extraordinary filopodia elongation results from the transport of espin 1 to the plus ends of F-actin by myosin IIIa and depends on espin 1 WH2 activity. This study provides the basis for understanding the role of myosin IIIa and espin 1 in regulating stereocilia length, and presents a physiological example where myosins can boost elongation of actin protrusions by transporting actin regulatory factors to the plus ends of actin filaments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.