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
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.
- Laboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
- Department of Biology, University of Maryland, College Park, MD 20742, USA.
- Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
- Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
- Current address: Consorzio Mario Negri Sud, Department of Cell Biology and Oncology, Santa Maria Imbaro, Chieti, Italy 66030.
- These authors contributed equally to the work.
Correspondence to: Bechara Kachar1 e-mail: kacharb@nidcd.nih.gov
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