Collapsin response mediator protein-4 regulates F-actin bundling

Rosslenbroich, Volker; Dai, Lingsong; Baader, Stephan L.; Noegel, Angelika A.; Gieselmann, Volkmar; Kappler, Joachim

doi:10.1016/j.yexcr.2005.08.005

Cited by 108 publications

(114 citation statements)

References 54 publications

(65 reference statements)

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“…6C). Previous findings have ascribed actin bundling activity to the carboxyl terminus of CRMP4 in vitro, thus we further investigated the possibility that EB3 dynamics may be regulated by coordinated activity of actin and microtubules by CRMP4 (27).…”

Section: Crmp4 Promotes Growth Cone Spreading and Axonmentioning

confidence: 99%

“…In addition, the CRMP4 isoform binds directly to F-actin and organizes F-actin into bundles in vitro. CRMP4 is also the sole CRMP isoform that can bind to RhoA, a key regulator of the actin cytoskeleton (27,28). In zebrafish, CRMP4 function is important for proper positioning of neural crest cells and caudal primary motor neurons, whereas in the mouse, CRMP4 supports proper bifurcation of apical dendrites (29 -31).…”

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confidence: 99%

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Collapsin Response Mediator Protein 4 Regulates Growth Cone Dynamics through the Actin and Microtubule Cytoskeleton

Khazaei

Girouard

Alchini

et al. 2014

Journal of Biological Chemistry

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Background: Intricate regulation of the growth cone cytoskeleton controls growth cone dynamics. Results: Loss of CRMP4 disrupts growth cone cytoskeletal dynamics, growth cone expansion, and axon growth. Conclusion: CRMP4 regulates both the actin and microtubule growth cone cytoskeleton. Significance: CRMP4 plays a critical role in regulating cytoskeletal dynamics underlying growth cone properties.

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Section: Crmp4 Promotes Growth Cone Spreading and Axonmentioning

confidence: 99%

mentioning

confidence: 99%

Collapsin Response Mediator Protein 4 Regulates Growth Cone Dynamics through the Actin and Microtubule Cytoskeleton

Khazaei

Girouard

Alchini

et al. 2014

Journal of Biological Chemistry

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“…CRMPs have been broadly implicated in the regulation of microtubule polymerization, actin bundling, and endocytosis, three processes that influence growth cone dynamics and neurite outgrowth (Fukata et al, 2002b;Nishimura et al, 2003;Rosslenbroich et al, 2005). To gain insight into how CRMP4b may influence neurite outgrowth inhibition, we assessed the distribution of CRMP4b in DRG growth cones.…”

Section: Crmp4b Affects the Growth Cone Actin Cytoskeletonmentioning

confidence: 99%

“…The localization of CRMP4b within the growth cone is consistent with a role in microtubule or actin dynamics. However, the filopodial and branching phenotypes promoted by CRMP4b overexpression suggest that CRMP4b may affect neuronal phenotype through an actin-based mechanism, an important observation because CRMPs have been implicated in modulating both microtubule and actin dynamics (Fukata et al, 2002a;Rosslenbroich et al, 2005). Although we cannot rule out the possibility that the fusion proteins may behave differently from native CRMP4b, both CRMP4b-V5 and CRMP4b-GFP have similar distributions to endogenous CRMP and promote similar growth cone phenotypes, suggesting that CRMP4b functionally interacts mainly with the actin cytoskeleton.…”

Section: Crmp4b Affects the Growth Cone Actin Cytoskeletonmentioning

confidence: 99%

“…CRMP2 mediates growth cone collapse in response to the repulsive guidance cue semaphorin3A (Sema3A) (Goshima et al, 1995), and CRMP2 and CRMP4 influence neurite outgrowth (Minturn et al, 1995;Quinn et al, 1999Quinn et al, , 2003Yoshimura et al, 2005). Mechanistically, CRMP2 can bind to tubulin heterodimers and organizes microtubule assembly to establish axon-dendrite fate during development (Fukata et al, 2002b;Arimura et al, 2005), and CRMP4 can promote F-actin bundling (Rosslenbroich et al, 2005). Also, a role for CRMP2 in endocytosis has been described previously (Nishimura et al, 2003), and an association between CRMP4b and intersectin, an endocytic-exocytic adaptor protein, is consistent with an endocytic role for this isoform (Quinn et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Identification of CRMP4 as a Convergent Regulator of Axon Outgrowth Inhibition

Alabed¹,

Pool²,

Tone³

et al. 2007

J. Neurosci.

132

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Myelin-associated inhibitors (MAIs) and chondroitin sulfate proteoglycans (CSPGs) contribute to failed regeneration after neuronal injury. MAIs and CSPGs stimulate intracellular signals including the activation of RhoA and Rho kinase to block axonal extension through targeted modifications to the cytoskeleton. RhoA and ROCK are promising targets for therapeutic intervention to promote CNS repair; however, their ubiquitous expression will limit the specificity of drugs targeted to these molecules. We have identified the cytosolic phosphoprotein CRMP4b (collapsin-response mediator protein 4b) as a protein that physically and functionally interacts with RhoA to mediate neurite outgrowth inhibition. Short interfering RNA-mediated knockdown of CRMP4 promotes neurite outgrowth on myelin substrates, indicating a critical role for CRMP4 in neurite outgrowth inhibition. Disruption of CRMP4b-RhoA binding with a competitive inhibitor attenuates neurite outgrowth inhibition on myelin and aggrecan substrates. Stimulation of neuronal growth cones with Nogo leads to colocalization of CRMP4b and RhoA at discrete regions within the actin-rich central and peripheral domains of the growth cone, indicative of a potential function in cytoskeletal rearrangements during neurite outgrowth inhibition. Together, these data indicate that a RhoA-CRMP4b complex forms in response to inhibitory challenges in the growth cone environment and regulates cytoskeletal dynamics at distinct sites necessary for axon outgrowth inhibition. Competitive inhibition of CRMP4b-RhoA binding suggests a novel, highly specific therapeutic avenue for promoting regeneration after CNS injury.

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CRMP4 suppresses apical dendrite bifurcation of CA1 pyramidal neurons in the mouse hippocampus

Niisato

Nagai

Yamashita

et al. 2012

Developmental Neurobiology

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Collapsin response mediator proteins (CRMPs) are a family of cytosolic phosphoproteins that consist of 5 members (CRMP 1-5). CRMP2 and CRMP4 regulate neurite outgrowth by binding to tubulin heterodimers, resulting in the assembly of microtubules. CRMP2 also mediates the growth cone collapse response to the repulsive guidance molecule semaphorin-3A (Sema3A). However, the role of CRMP4 in Sema3A signaling and its function in the developing mouse brain remain unclear. We generated CRMP4À/À mice in order to study the in vivo function of CRMP4 and identified a phenotype of proximal bifurcation of apical dendrites in the CA1 pyramidal neurons of CRMP4À/À mice. We also observed increased dendritic branching in cultured CRMP4À/À hippocampal neurons as well as in cultured cortical neurons treated with CRMP4 shRNA. Sema3A induces extension and branching of the dendrites of hippocampal neurons; however, these inductions were compromised in the CRMP4À/À hippocampal neurons. These results suggest that CRMP4 suppresses apical dendrite bifurcation of CA1 pyramidal neurons in the mouse hippocampus and that this is partly dependent on Sema3A signaling.

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Collapsin response mediator protein-4 regulates F-actin bundling

Cited by 108 publications

References 54 publications

Collapsin Response Mediator Protein 4 Regulates Growth Cone Dynamics through the Actin and Microtubule Cytoskeleton

Collapsin Response Mediator Protein 4 Regulates Growth Cone Dynamics through the Actin and Microtubule Cytoskeleton

Identification of CRMP4 as a Convergent Regulator of Axon Outgrowth Inhibition

CRMP4 suppresses apical dendrite bifurcation of CA1 pyramidal neurons in the mouse hippocampus

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