| Autor: |
Salles FT, Merritt RC Jr, Manor U, Dougherty GW, Sousa AD, Moore JE, Yengo CM, Dosé AC, Kachar B |
| Jazyk: |
angličtina |
| Zdroj: |
Nature cell biology [Nat Cell Biol] 2009 Apr; Vol. 11 (4), pp. 443-50. Date of Electronic Publication: 2009 Mar 15. |
| DOI: |
10.1038/ncb1851 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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