ERM proteins regulate growth cone responses to Sema3A

Mintz, C. David; Carcea, Ioana; McNickle, D.G.; Dickson, Tracey C.; Ge, Yongchao; Salton, Stephen R.J.; Benson, Deanna L.

doi:10.1002/cne.21799

Cited by 31 publications

(59 citation statements)

References 118 publications

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“…L1 endocytosis is involved in downregulating the levels of the semaphorin3A coreceptor, neuropilin-1 (Bechara et al 2007). The ability of L1 to bind ERM proteins via its cytoplasmic tail is important in these semaphorin-mediated events (Mintz et al 2008). The endocytosis of the L1-neuropilin-1 complex also leads to local signaling and disassembly of focal adhesions (Bechara et al 2008).…”

Section: Regulation Of Local Endocytosismentioning

confidence: 99%

Trafficking Guidance Receptors

Winckler

Mellman²

2010

Cold Spring Harbor Perspectives in Biology

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Wiring of the brain relies initially on the correct outgrowth of axons to reach the appropriate target area for innervation. A large number of guidance receptors present in the plasma membrane of axonal growth cones and elsewhere on the neuron read and execute directional cues present in the extracellular environment of the navigating growth cone. The exact timing, levels, and localization of expression of the guidance receptors in the plasma membrane therefore determine the outcome of guidance decisions. Many guidance receptors are localized in exquisitely precise spatial and temporal patterns. The cellular mechanisms ensuring these localization patterns include spatially accurate sorting after synthesis in the secretory pathway, retrieval of inappropriately expressed receptors by endocytosis followed by degradation or recycling, and restriction of diffusion. This article will discuss the machinery and regulation underlying the restricted distribution of membrane receptors, focusing on the currently best-studied example, the L1 cell adhesion molecule. In addition to the longrange mechanisms ensuring appropriate localization, the same mechanisms can act locally to adjust levels and localization of receptors. These local mechanisms are regulated by ligand binding and subsequent activation of local signaling cascades. It is likely that the localization of all guidance receptors is regulated by a combination of sorting, retrieval, recycling and retention, similar to the ones we discuss here for L1.

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Section: Regulation Of Local Endocytosismentioning

confidence: 99%

Trafficking Guidance Receptors

Winckler

Mellman²

2010

Cold Spring Harbor Perspectives in Biology

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“…Experimental evidence has been provided that the phosphorylation and dephosphorylation of Tyr1176 controls cycles of L1CAM endocytosis and cell surface trafficking in the advancing growth cone (Kamiguchi and Lemmon 2000;Kamiguchi and Yoshihara 2001;Schaefer et al 2002). Doubleimmunolabeling has revealed distinct localizations of these ERM and AP-2 proteins in growth cones of cortical neurons suggesting the lack of competitive binding of these molecules to the cytoplasmic domain of L1CAM (Mintz et al 2008). One possible explanation might be that lateral redistribution of L1CAM to distinct membrane microdomains allows association either with ERM or AP-2 proteins (Fig.…”

Section: L1cam and Erm Proteinsmentioning

confidence: 96%

“…2b). Dominant-negative ezrin also inhibits Sema 3A-mediated growth cone collapse (Mintz et al 2008) suggesting a cooperative mode of interaction for L1CAM and ezrin in this process. Studies of growth cones of dorsal root ganglion cells indicate that Sema 3A induces the dephosphorylation of ERM proteins (Gallo 2008).…”

Section: L1cam and Erm Proteinsmentioning

confidence: 97%

“…This effect has also been observed in growth cones from cortical neurons. In addition, the dephosphorylation of ezrin causes enhanced internalization of L1CAM and Nrp-1 in these cells (Mintz et al 2008). After the endocytosis of L1CAM/Nrp-1, ezrin has been hypothesized to become reactivated, thereby again stabilizing L1CAM/Nrp-1 in the plasma membrane and mediating their linkage to the actin cytoskeleton (Mintz et al 2008).…”

Section: L1cam and Erm Proteinsmentioning

confidence: 99%

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Role of L1CAM for axon sprouting and branching

Schäfer

Frotscher²

2012

Cell Tissue Res

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The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during the last few decades has identified axon sprouting as an anatomical correlate for the regenerative capability of the CNS to establish new connections. The immunoglobulin superfamily member L1CAM has been shown to promote the capability of neurons for regenerative axon sprouting and to improve behavioral outcomes after CNS injury. Here, we discuss the cell-autonomous role of L1CAM for axon sprouting in experimental rodent injury models and highlight the molecular interactions of L1CAM with ankyrins, ezrin-radixin-moesin proteins and the Sema3A/Neuropilin ligand-receptor complex in the context of axonal branching.

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“…Subsequently, phosphorylation at the C-terminal threonine site (T567 ezrin, T564 radixin, and T558 moesin) stabilizes an open conformation and promotes actin-binding activity [25]. ERM proteins act as essential mediators of various extracellular signals affecting growth cone morphology and neurite development [26][27][28][29]. It has been reported that migrating neuroblasts in the RMS also highly express ERM molecules such as radixin [30,31], raising the possibility that ERM molecules are involved in the regulation of neuroblast migration in the RMS.…”

Section: Introductionmentioning

confidence: 99%

Function of Ezrin-Radixin-Moesin Proteins in Migration of Subventricular Zone-Derived Neuroblasts Following Traumatic Brain Injury

Moon

Kim

et al. 2013

Stem Cells

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Throughout life, newly generated neuroblasts from the subventricular zone migrate toward the olfactory bulb through the rostral migratory stream. Upon brain injury, these migrating neuroblasts change their route and begin to migrate toward injured regions, which is one of the regenerative responses after brain damage. This injury-induced migration is triggered by stromal cell-derived factor 1 (SDF1) released from microglia near the damaged site; however, it is still unclear how these cells transduce SDF1 signals and change their direction. In this study, we found that SDF1 promotes the phosphorylation of ezrin-radixin-moesin (ERM) proteins, which are key molecules in organizing cell membrane and linking signals from the extracellular environment to the intracellular actin cytoskeleton. Blockade of ERM activation by overexpressing dominant-negative ERM (DN-ERM) efficiently perturbed the migration of neuroblasts. Considering that DN-ERM-expressing neuroblasts failed to maintain proper migratory cell morphology, it appears that ERM-dependent regulation of cell shape is required for the efficient migration of neuroblasts. These results suggest that ERM activation is an important step in the directional migration of neuroblasts in response to SDF1-CXCR4 signaling following brain injury.

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ERM proteins regulate growth cone responses to Sema3A

Cited by 31 publications

References 118 publications

Trafficking Guidance Receptors

Trafficking Guidance Receptors

Role of L1CAM for axon sprouting and branching

Function of Ezrin-Radixin-Moesin Proteins in Migration of Subventricular Zone-Derived Neuroblasts Following Traumatic Brain Injury

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