3 MyTH4-FERM myosins in addition to Myo10: MYO7A, the gene that is mutated in Usher syndrome 1b deaf-blindness; MYO7B, a component of an adhesion complex at the tips of microvilli; and MYO15A, a myosin that localizes to the tips of inner ear stereocilia and that is mutated in DFNB3 deafness. The head domains of the other MyTH4-FERM myosins expressed in human exhibit at most 45% overall amino acid sequence identity with Myo10 and their tail domains each contain 2 MyTH4-FERM domains instead of the 3 PH domains and 1 MyTH4-FERM domain in Myo10. Cellular function Myo10 can localize to the tips of filopodia, a property most other myosins lack. When Myo10 was tagged with Green Fluorescent Protein (GFP) and expressed in cells, small puncta of GFP-Myo10 were observed moving forward within filopodia towards the tip at rates of ~100 nm/s. Imaging with single-molecule sensitivity revealed similar movements of individual Myo10 dimers at rates of ~600-1400 nm/s. GFP-Myo10 also moves rearward in filopodia at retrograde flow rates of ~15 nm/s. These observations led to the hypothesis that Myo10 molecules use their motor activity to move themselves rapidly forward along filopodial actin filaments and can bind to filopodial actin filaments to be carried slowly rearward by retrograde actin flow. This “intrafilopodial motility” of Myo10 has led to suggestions that Myo10 functions as a motor protein for transporting cargos within filopodia. Myo10 also has important functions in the formation and/or stabilization of filopodia, with Myo10 overexpression increasing the number and length of filopodia, while knockdown or knockout of Myo10 decreases filopodia. Myo10 also has important functions in cell division, particularly in mitotic spindle orientation. Myo10 is also required to cluster the excess centrosomes that are a hallmark of cancer cells, a process of great interest because cancer cells need to cluster their centrosomes to successfully divide. Role in disease Growing evidence demonstrates that Myo10 has important roles in cancer. In addition to its role in clustering the excess centrosomes of cancer cells, Myo10 is a key component of invadopodia, filopodia-related protrusions that cancer cells use to invade their surroundings. Several microRNAs that suppress cancer cell invasion have also been reported to act in part by targeting the Myo10 mRNA. Knockout or knockdown of Myo10 is reported to suppress cancer cell invasion or spread in experimental models of breast cancer, lung cancer, and glioma, where knockout of Myo10 also increased the effectiveness of an