Switching between Microtubule- and Actin-Based Transport Systems in Melanophores Is Controlled by cAMP Levels

Rodionov, Vladimir; Yi, Julie; Kashina, Anna; Oladipo, Abiola; Gross, Steven P.

doi:10.1016/j.cub.2003.10.027

Cited by 110 publications

(139 citation statements)

References 46 publications

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“…Because the same seems true here, virus particles may be recruiting a complete bidirectional transport apparatus similar to one used in those systems. Significantly, in two of the previously described systems, there is a key difference: in the melanophores, transport is controlled by a global signal (cAMP͞PKA) whereas, for the lipid droplets, a globally acting directionality factor (Halo) determines the amount of plus-end motion of all lipid droplets in the embryo (44,45). In contrast, global changes in the infected cell are not responsible for differential capsid motion during egress versus entry: the ability of capsids newly deposited into the axon during superinfection to undergo typical retrograde motion indicates that local changes in capsid structure modulate appropriate targeting.…”

Section: Discussionmentioning

confidence: 99%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

133

177

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The core structures of many viruses move within cells by association with host cytoskeletal motor proteins; however, the mechanisms by which intracellular viral particles are transported toward sites of replication or the cell periphery at distinct stages of infection remain to be understood. The regulation of herpesvirus directional transport in sensory neurons was examined by tracking individual viral capsids within axons at multiple frames per s. After entry into axons, capsids underwent bidirectional and saltatory movement to the cell body independently of endosomes. A comparison of entry transport to a previous analysis of capsid axonal transport during egress revealed that capsid targeting in and out of cells occurs by modulation of plus-end, but not minus-end, motion. Entry transport was unperturbed by the presence of egressing virus from a prior infection, indicating that transport direction is not modulated globally by viral gene expression, but rather directly by a component of the viral particle.virus ͉ neuron

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Section: Discussionmentioning

confidence: 99%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

133

177

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“…For example, during aggregation of melanosomes in mouse melanocytes and Xenopus laevis melanophores, the dynein/microtubule system counteracts the MyoVa/actin system, forcing the melanosomes to switch from the actin to the microtubule network so they can be transported toward the cell center (3,57). In contrast, when melanosomes disperse toward the cell periphery, the MyoVa/actin system wins over the dynein/microtubule system and switches melanosomes to the actin network (3,38,58). However, regulatory mechanisms that govern the directionality of the transport between the two cytoskeletal networks remained unclear.…”

Section: Microtubules Compete Efficiently For Mlph Binding In the Prementioning

confidence: 99%

Myosin Va’s adaptor protein melanophilin enforces track selection on the microtubule and actin networks in vitro

Oberhofer

Spieler

Rosenfeld

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Pigment organelles, or melanosomes, are transported by kinesin, dynein, and myosin motors. As such, melanosome transport is an excellent model system to study the functional relationship between the microtubule-and actin-based transport systems. In mammalian melanocytes, it is well known that the Rab27a/melanophilin/myosin Va complex mediates actin-based transport in vivo. However, pathways that regulate the overall directionality of melanosomes on the actin/microtubule networks have not yet been delineated. Here, we investigated the role of PKA-dependent phosphorylation on the activity of the actin-based Rab27a/melanophilin/myosin Va transport complex in vitro. We found that melanophilin, specifically its C-terminal actin-binding domain (ABD), is a target of PKA. Notably, in vitro phosphorylation of the ABD closely recapitulated the previously described in vivo phosphorylation pattern. Unexpectedly, we found that phosphorylation of the ABD affected neither the interaction of the complex with actin nor its movement along actin tracks. Surprisingly, the phosphorylation state of melanophilin was instead important for reversible association with microtubules in vitro. Dephosphorylated melanophilin preferred binding to microtubules even in the presence of actin, whereas phosphorylated melanophilin associated with actin. Indeed, when actin and microtubules were present simultaneously, melanophilin's phosphorylation state enforced track selection of the Rab27a/melanophilin/ myosin Va transport complex. Collectively, our results unmasked the regulatory dominance of the melanophilin adaptor protein over its associated motor and offer an unexpected mechanism by which filaments of the cytoskeletal network compete for the moving organelles to accomplish directional transport on the cytoskeleton in vivo.melanophilin | myosin Va | intracellular transport | transport regulation

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“…Similarly, synaptic stimulation in Aplysia neurons strongly enhanced the transport of Ap-eEF1A mRNAs to axonal processes, while its transcripts accumulated around the nucleus when the stimulation was restricted to the cell body (Giustetto et al, 2003). Conceivably, activity-mediated tagging of cytoskeleton structures by PKA or another activity-dependent kinase might enhance the transport of mRNAs and proteins to dendrites containing those synapses recently stimulated (Kotz and McNiven, 1994;Luo, 2002;Rodionov et al, 2003;Sanchez et al, 2000). Interestingly, recent studies in cultured neurons have demonstrated that post-Golgi membrane trafficking is polarized toward specific dendrites and small Golgi outposts partition selectively into longer dendrites and concentrate at branchpoints (Horton et al, 2005).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Barco

Armentia

Alarcón

2008

Neuroscience & Biobehavioral Reviews

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Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited ten years later, Neuroscience and Biobehavioral Reviews (2008Reviews ( ), doi:10.1016Reviews ( /j.neubiorev.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A c c e p t e d m a n u s c r i p t A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 2 Abstract A decade ago, the synaptic tagging hypothesis was proposed to explain how newly synthesized plasticity products can be specifically targeted to active synapses. A growing number of studies have validated the seminal findings that gave rise to this model, as well as contributed to unveil and expand the range of mechanisms underlying late-associativity and neuronal computation.Here, we will review what it was learnt during this past decade regarding the cellular and molecular mechanisms underlying synaptic tagging and synaptic capture. The accumulated experimental evidence has widened the theoretical framework set by the synaptic tagging and capture (STC) model and introduced concepts that were originally considered part of alternative models for explaining synapse-specific LTP. As a result, we believe that the STC model, now improved and expanded with these new ideas and concepts, still represents the most compelling hypothesis to explain late-associativity in synapse-specific plasticity processes. We will also discuss the impact of this model in our view of the integrative capability of neurons and associative learning. wordsKeywords: synaptic plasticity; LTP; associative learning; neuronal computation; synaptic tagging; synaptic capture; metaplasticity A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 3 Contents

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Switching between Microtubule- and Actin-Based Transport Systems in Melanophores Is Controlled by cAMP Levels

Abstract: We conclude that the switching of pigment granules between the two major cytoskeletal systems is independent of the densities of MT or AF but is tightly controlled by signaling events.

Cited by 110 publications

References 46 publications

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Myosin Va’s adaptor protein melanophilin enforces track selection on the microtubule and actin networks in vitro

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

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