Neuronal myosin-X is upregulated after peripheral nerve injury and mediates laminin-induced growth of neurites

Plantman, Stefan; Zelano, Johan; Novikova, Liudmila N.; Novikov, Lev N.; Cullheim, Staffan

doi:10.1016/j.mcn.2013.04.001

Cited by 13 publications

(11 citation statements)

References 28 publications

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“…Although these filopodia did not contain detectable MyoX at the tips, MyoX was concentrated in growth cones (Fig. 6), similarly to what was observed in spinal motorneurons (Plantman et al, 2013). It is possible that the function of MyoX in growth cones is different from its function as an organizer of the filopodia tip complex.…”

Section: Discussionsupporting

confidence: 70%

Dopamine transporter is enriched in filopodia and induces filopodia formation

Caltagarone

Sorkin

2015

Molecular and Cellular Neuroscience

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Dopamine transporter (DAT, SLC6A3) controls dopamine (DA) neurotransmission by mediating re-uptake of extracellular DA into DA neurons. DA uptake depends on the amount of DAT at the cell surface, and is therefore regulated by DAT subcellular distribution. Hence we used spinning disc confocal microscopy to demonstrate DAT localization in membrane protrusions that contained filamentous actin and myosin X (MyoX), a molecular motor located in filopodia tips, thus confirming that these protrusions are filopodia. DAT was enriched in filopodia. In contrast, R60A and W63A DAT mutants with disrupted outward-facing conformation were not accumulated in filopodia, suggesting that this conformation is necessary for DAT filopodia targeting. Three independent approaches of filopodia counting showed that DAT expression leads to an increase in the number of filopodia per cell, indicating that DAT can induce filopodia formation. Depletion of MyoX by RNA interference resulted in a significant loss of filopodia but did not completely eliminate filopodia, implying that DAT-enriched filopodia can be formed without MyoX. In cultured postnatal DA neurons MyoX was mainly localized to growth cones that displayed highly dynamic DAT-containing filopodia. We hypothesize that the concave shape of the DAT molecule functions as the targeting determinant for DAT accumulation in outward-curved membrane domains, and may also allow high local concentrations of DAT to induce an outward membrane bending. Such targeting and membrane remodeling capacities may be part of the mechanism responsible for DAT enrichment in the filopodia and its targeting to the axonal processes of DA neurons.

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Section: Discussionsupporting

confidence: 70%

Dopamine transporter is enriched in filopodia and induces filopodia formation

Caltagarone

Sorkin

2015

Molecular and Cellular Neuroscience

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“…In the brain, Myo10 is upregulated during nerve regeneration following sciatic axotomy (Tanabe et al, 2003) or following peripheral nerve injury (Plantman et al, 2013). In addition, Myo10 is highly regulated during development of the nervous system and exists in two forms (Sousa et al, 2006), the fulllength and the 'headless' isoform, which lacks the motor activity and is differently regulated during development (Sousa et al, 2006;Raines et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Myo10 is a key regulator of TNT formation in neuronal cells

Gousset

Marzo

Commère

et al. 2013

Journal of Cell Science

148

212

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SummaryCell-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.

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“…High amounts of actin are found in synapses and dendritic spines were it is crucial for synapse function (Rust and Maritzen, 2015), the latter being formed by dendritic filopodia outgrowth (Fifkova, 1985;Landis et al, 1988;Matus et al, 1982)-an F-actin and myosin X dependent process (Kerber and Cheney, 2011;Plantman et al, 2013). In addition in central synapses neurotransmitter release at is regulated by Factin (Morales et al, 2000) The actomyosin cortex actively modulates plasma membrane properties…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Membrane shaping by actin and myosin during regulated exocytosis

Papadopulos

2017

Molecular and Cellular Neuroscience

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The cortical actin network in neurosecretory cells is a dense mesh of actin filaments underlying the plasma membrane. Interaction of actomyosin with vesicular membranes or the plasma membrane is vital for tethering, retention, transport as well as fusion and fission of exo-and endocytic membrane structures. During regulated exocytosis the cortical actin network undergoes dramatic changes in morphology to accommodate vesicle docking, fusion and replenishment. Most of these processes involve plasma membrane Phosphoinositides (PIP) and investigating the interactions between the actin cortex and secretory structures has become a hotbed for research in recent years. Actin remodelling leads to filopodia outgrowth and the creation of new fusion sites in neurosecretory cells and actin, myosin and dynamin actively shape and maintain the fusion pore of secretory vesicles. Changes in viscoelastic properties of the actin cortex can facilitate vesicular transport and lead to docking and priming of vesicle at the plasma membrane. Small GTPase actin mediators control the state of the cortical actin network and influence vesicular access to their docking and fusion sites. These changes potentially affect membrane properties such as tension and fluidity as well as the mobility of embedded proteins and could influence the processes leading to both exo-and endocytosis. Here we discuss the multitudes of actin and membrane interactions that control successive steps underpinning regulated exocytosis.

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Neuronal myosin-X is upregulated after peripheral nerve injury and mediates laminin-induced growth of neurites

Cited by 13 publications

References 28 publications

Dopamine transporter is enriched in filopodia and induces filopodia formation

Dopamine transporter is enriched in filopodia and induces filopodia formation

Myo10 is a key regulator of TNT formation in neuronal cells

Membrane shaping by actin and myosin during regulated exocytosis

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