A role of MAP1B in Reelin-dependent Neuronal Migration

González-Billault, Christian; Rı́o, José Antonio del; Ureña, Jesús; Jiménez-Mateos, Eva M.; Barallobre, Marı́a José; Pascual, Marta; Pujadas, Lluı́s; Simó, Sergi; Torre, Anna La; Gavı́n, Rosalina; Wandosell, Francisco; Soriano, Eduardo; Ávila, Jesús

doi:10.1093/cercor/bhh213

Cited by 106 publications

(75 citation statements)

References 85 publications

(151 reference statements)

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“…Moreover, Reelin signaling induces the phosphorylation of GSK3b at its tyrosine residue, leading to its activation. Activated GSK3b functions synergistically with CDK5 to phosphorylate another microtubule associated protein, MAP1B (Gonzalez-Billault et al 2005). Phosphorylation of MAP1B is believed to regulate microtubule stability and the cross talk between microtubules and actin filaments in axonal growth cones (Kawauchi et al 2005).…”

Section: Guiding Neuronal Cell Migrationsmentioning

confidence: 99%

Guiding Neuronal Cell Migrations

Marı́n¹,

Valiente²,

Ge³

et al. 2010

Cold Spring Harbor Perspectives in Biology

359

351

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Neuronal migration is, along with axon guidance, one of the fundamental mechanisms underlying the wiring of the brain. As other organs, the nervous system has acquired the ability to grow both in size and complexity by using migration as a strategy to position cell types from different origins into specific coordinates, allowing for the generation of brain circuitries. Guidance of migrating neurons shares many features with axon guidance, from the use of substrates to the specific cues regulating chemotaxis. There are, however, important differences in the cell biology of these two processes. The most evident case is nucleokinesis, which is an essential component of migration that needs to be integrated within the guidance of the cell. Perhaps more surprisingly, the cellular mechanisms underlying the response of the leading process of migrating cells to guidance cues might be different to those involved in growth cone steering, at least for some neuronal populations.

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Section: Guiding Neuronal Cell Migrationsmentioning

confidence: 99%

Guiding Neuronal Cell Migrations

Marı́n¹,

Valiente²,

Ge³

et al. 2010

Cold Spring Harbor Perspectives in Biology

359

351

View full text Add to dashboard Cite

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“…MAP1b is present in axons, soma, and dendrites, although it is especially prominent in extending axons and their growth cones (39, 78 -82). This microtubule-associated protein regulates early axonal outgrowth and establishment of neuronal polarity by modulating microtubule dynamics through its capacity to bind the microtubule lattice and regulate microtubule assembly and stability in in vitro and in vivo models (83)(84)(85)(86)(87)(88)(89)(90)(91).…”

Section: Kidins220/arms Associates With and Modulates The Activity Ofmentioning

confidence: 99%

“…This phosphorylation regulates MAP1b ability to maintain a more dynamically unstable microtubule population in the distal part of the axon when exposed to neurotrophin, netrin, and reelin (88,(93)(94)(95)(96). The rise in total MAP1b HC after Kidins220/ARMS knockdown could simply reflect an increase in axonal structural proteins to produce higher number of axons, and the phosphorylation decrease would promote axonal microtubule stabilization and outgrowth.…”

Section: Kidins220/arms Associates With and Modulates The Activity Ofmentioning

confidence: 99%

Kidins220/ARMS Modulates the Activity of Microtubule-regulating Proteins and Controls Neuronal Polarity and Development

Higuero

Sánchez‐Ruiloba

Doglio

et al. 2010

Journal of Biological Chemistry

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In order for neurons to perform their function, they must establish a highly polarized morphology characterized, in most of the cases, by a single axon and multiple dendrites. Herein we find that the evolutionarily conserved protein Kidins220 (kinase D-interacting substrate of 220-kDa), also known as ARMS (ankyrin repeat-rich membrane spanning), a downstream effector of protein kinase D and neurotrophin and ephrin receptors, regulates the establishment of neuronal polarity and development of dendrites. Kidins220/ARMS gain and loss of function experiments render severe phenotypic changes in the processes extended by hippocampal neurons in culture. Although Kidins220/ARMS early overexpression hinders neuronal development, its down-regulation by RNA interference results in the appearance of multiple longer axon-like extensions as well as aberrant dendritic arbors. We also find that Kidins220/ARMS interacts with tubulin and microtubule-regulating molecules whose role in neuronal morphogenesis is well established (microtubule-associated proteins 1b, 1a, and 2 and two members of the stathmin family). Importantly, neurons where Kidins220/ARMS has been knocked down register changes in the phosphorylation activity of MAP1b and stathmins. Altogether, our results indicate that Kidins220/ARMS is a key modulator of the activity of microtubuleregulating proteins known to actively regulate neuronal morphogenesis and suggest a mechanism by which it contributes to control neuronal development.Neuronal differentiation comprises several steps, among which the acquirement of a polarized axon-dendrite phenotype, with the corresponding asymmetrical distribution of proteins, is crucial. The morphological changes, followed by a neuron in order to polarize and form a single axon and multiple dendrites, are triggered by signaling cascades evoked by both intracellular and extracellular cues (1-4).Embryonic hippocampal neurons in culture constitute a model to study the mechanisms governing the establishment of polarity (2, 5, 6). These neurons undergo clear morphological changes during in vitro polarization. First, neurons attach to the plate and form lamellipodia and filopodia (stage 1). After several hours, they extend several minor immature neurites of apparent equivalent nature (stage 2) until one of these minor processes extends rapidly and becomes the axon (stage 3). The remaining neurites develop into dendrites (stage 4), after which neurons become morphologically and functionally mature (stage 5) (5, 6).During the early events of the establishment of polarity in this model, differences in local actin polymerization among the immature neurites play a crucial role in axonal determination (5, 7). In a similar manner, microtubule dynamics influence neuronal polarization, because local microtubule stabilization in one neurite specifies an axonal fate (8). Other known regulators of neuronal polarity and axon specification include proteins involved in polarized trafficking (4, 9, 10). However, how these different molecules are linked to t...

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“…Furthermore, Reelin can also induce MAP1B phosphorylation through GSK-3β activation. MAP1B function is involved in formation of brain laminated areas, therefore, Reelin can modulate neuronal guidance through post-translational modifications of MAP1B [34]. These two examples show how Reelin can act coordinately to locally regulate the assembly of actin microfilaments and microtubules ( Figure 1A).…”

Section: Reelin In Neurodevelopmentmentioning

confidence: 97%