期刊
NATURE CELL BIOLOGY
卷 11, 期 4, 页码 443-U180出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1851
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资金
- NIDCD
- DIR
- NIH [EY003575, EY016419]
Two proteins implicated in inherited deafness, myosin IIIa(1), a plus-end-directed motor(2), and espin(3-6), an actin-bundling protein containing the actin-monomer- binding motif WH2, have been shown to influence the length of mechanosensory stereocilia(7,8). Here we report that espin 1, an ankyrin repeat-containing isoform of espin(6), 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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