Letter abstract


Nature Cell Biology 11, 443 - 450 (2009)
Published online: 15 March 2009 | doi:10.1038/ncb1851

Myosin IIIa boosts elongation of stereocilia by transporting espin 1 to the plus ends of actin filaments

Felipe T. Salles1,6, Raymond C. Merritt, Jr1,2,6, Uri Manor1, Gerard W. Dougherty1,5, Aurea D. Sousa1, Judy E. Moore3, Christopher M. Yengo3, Andréa C. Dosé4 & Bechara Kachar1

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Two proteins implicated in inherited deafness, myosin IIIa1, a plus-end-directed motor2, and espin3, 4, 5, 6, an actin-bundling protein containing the actin-monomer-binding motif WH2, have been shown to influence the length of mechanosensory stereocilia7, 8. Here we report that espin 1, an ankyrin repeat-containing isoform of espin6, 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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  1. Laboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
  2. Department of Biology, University of Maryland, College Park, MD 20742, USA.
  3. Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
  4. Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
  5. Current address: Consorzio Mario Negri Sud, Department of Cell Biology and Oncology, Santa Maria Imbaro, Chieti, Italy 66030.
  6. These authors contributed equally to the work.

Correspondence to: Bechara Kachar1 e-mail: kacharb@nidcd.nih.gov



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