Key result
Myo10 protein expression increases the number of tunneling nanotubes and the transfer of vesicles between co-cultured neuronal CAD cells.
Myo10 is a key regulator of tunneling nanotube formation in neuronal cells, driving dorsal filopodia independent of integrin and N-cadherin binding.
Preclinical cell data only; leaves open Myo10 as a therapeutic target for neuronal vesicle transfer pending in vivo validation.
Cell-to-cell communication is essential in multicellular organisms. Tunneling nanotubes (TNTs) have emerged as a new type of intercellular spreading mechanism allowing the transport of various signals, organelles and pathogens. Here, we study the role of the unconventional molecular motor myosin-X (Myo10) in the formation of functional TNTs within neuronal CAD cells. Myo10 protein expression increases the number of TNTs and the transfer of vesicles between co-cultured cells. We also show that TNT formation requires both the motor and tail domains of the protein, and identify the F2 lobe of the FERM domain within the Myo10 tail as necessary for TNT formation. Taken together, these results indicate that, in neuronal cells, TNTs can arise from a subset of Myo10-driven dorsal filopodia, independent of its binding to integrins and N-cadherins. In addition our data highlight the existence of different mechanisms for the establishment and regulation of TNTs in neuronal cells and other cell types.
No takes yet. Share an insight, caveat, or question.
Gousset et al. (2013) studied this question. Myo10 protein expression was evaluated on Tunneling nanotube (TNT) formation and vesicle transfer. Myo10 protein expression increases the number of tunneling nanotubes and the transfer of vesicles between co-cultured neuronal CAD cells.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: