Critical Role of Collapsin Response Mediator Protein-associated Molecule CRAM for Filopodia and Growth Cone Development in Neurons

Hotta, Azusa; Inatome, Ryoko; Yuasa-Kawada, Junichi; Qin, Qingyu; Yamamura, Hirohei; Yanagi, Shigeru

doi:10.1091/mbc.e04-08-0679

Cited by 47 publications

(48 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We therefore examined the possibility that CRMP5 is involved in neurotrophin signaling. Since CRMP5 is expressed in Purkinje cells only after P14 (Bretin et al, 2005;Hotta et al, 2005) (Fig. 5), it is difficult to examine the effect of BDNF at such elaborate dendritic stage using culture system.…”

Section: Attenuated Response To Bdnf In Cultured Crmp5mentioning

confidence: 99%

“…5), it is difficult to examine the effect of BDNF at such elaborate dendritic stage using culture system. In contrast, CRMP5 is expressed in the early stages of hippocampal development (Hotta et al, 2005). We therefore used hippocampal neurons taken from early embryonic stage (E16.5) for primary culture neurons and examined the effect of BDNF regarding to primary dendrite formation (Cheung et al, 2007).…”

Section: Attenuated Response To Bdnf In Cultured Crmp5mentioning

confidence: 99%

“…CRMP5 plays an important role in regulating filopodia and growth cone morphology in neurons (Hotta et al, 2005). Like other types of CRMP family proteins, CRMP5 is expressed throughout the nervous system (Wang and Strittmatter, 1996;Fukada et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

Yamashita¹,

Mosinger²,

Roy³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

Collapsin response mediator protein 5 (CRMP5) is one of the CRMP members that expresses abundantly in the developing brain. To examine the in vivo function of CRMP5, we generated crmp5-deficient (crmp5 Ϫ/Ϫ ) mice. Anti-calbindin immunofluorescence studies of crmp5 Ϫ/Ϫ mice revealed aberrant dendrite morphology; specifically, a decrease in the size of soma and diameter of primary dendrite of the cerebellar Purkinje cells at postnatal day 21 (P21) and P28, but not at P14. Coincidentally, CRMP5 is detected in Purkinje cells at P21 and P28 from crmp5 ϩ/Ϫ mice. In cerebellar slices of crmp5 Ϫ/Ϫ mice, the induction of long-term depression of excitatory synaptic transmission between parallel fibers and Purkinje cells was deficient. Given that brain-derived neurotrophic factor (BDNF) plays major roles in dendritic development, we tried to elucidate the possible roles of CRMP5 in BDNF signaling. The effect of BDNF to induce dendritic branching was markedly attenuated in cultured crmp5 Ϫ/Ϫ neurons. Furthermore, CRMP5 was tyrosine phosphorylated when coexpressed with neurotrophic tyrosine kinase receptor type 2 (TrkB), a receptor for BDNF, in HEK293T cells. These findings suggest that CRMP5 is involved in the development, maintenance and synaptic plasticity of Purkinje cells.

show abstract

Section: Attenuated Response To Bdnf In Cultured Crmp5mentioning

confidence: 99%

Section: Attenuated Response To Bdnf In Cultured Crmp5mentioning

confidence: 99%

See 1 more Smart Citation

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

Yamashita¹,

Mosinger²,

Roy³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Whereas it is well established that CRMPs 1-5 promote axonal growth, neurite branching and growth-cone formation (Fukata et al, 2002;Hotta et al, 2005;Inagaki et al, 2001;Schmidt and Strittmatter, 2007), the role of CRMPs in sensory signaling is largely unexplored. Studies indicate that Sema 3A might produce its effects by causing opening of Ca 2+ channels (Behar et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Xuan

Schmutzler

Brittain

et al. 2009

Journal of Cell Science

129

157

View full text Add to dashboard Cite

Collapsin response mediator proteins (CRMPs) mediate signal transduction of neurite outgrowth and axonal guidance during neuronal development. Voltage-gated Ca2+ channels and interacting proteins are essential in neuronal signaling and synaptic transmission during this period. We recently identified the presynaptic N-type voltage-gated Ca2+ channel (Cav2.2) as a CRMP-2-interacting partner. Here, we investigated the effects of a functional association of CRMP-2 with Cav2.2 in sensory neurons. Cav2.2 colocalized with CRMP-2 at immature synapses and growth cones, in mature synapses and in cell bodies of dorsal root ganglion (DRG) neurons. Co-immunoprecipitation experiments showed that CRMP-2 associates with Cav2.2 from DRG lysates. Overexpression of CRMP-2 fused to enhanced green fluorescent protein (EGFP) in DRG neurons, via nucleofection, resulted in a significant increase in Cav2.2 current density compared with cells expressing EGFP. CRMP-2 manipulation changed the surface levels of Cav2.2. Because CRMP-2 is localized to synaptophysin-positive puncta in dense DRG cultures, we tested whether this CRMP-2-mediated alteration of Ca2+ currents culminated in changes in synaptic transmission. Following a brief high-K+-induced stimulation, these puncta became loaded with FM4-64 dye. In EGFP and neurons expressing CRMP-2–EGFP, similar densities of FM-loaded puncta were observed. Finally, CRMP-2 overexpression in DRG increased release of the immunoreactive neurotransmitter calcitonin gene-related peptide (iCGRP) by ∼70%, whereas siRNA targeting CRMP-2 significantly reduced release of iCGRP by ∼54% compared with control cultures. These findings support a novel role for CRMP-2 in the regulation of N-type Ca2+ channels and in transmitter release.

show abstract

“…Overexpression of CRMP2 in hippocampal neurons induced supernumerary axons (Inagaki et al, 2001), axon elongation (Cole et al, 2004) and increased axonal branching (Fukata et al, 2002), whereas its inhibition with a dominant-negative protein suppressed the formation of primary axons. Similarly, CRMP5 overexpression induced supernumerary growth cones and increased collateral axon branching, whereas its inhibition by siRNA led to a decrease in filopodia and growth cone formation (Hotta et al, 2005). CRMP5 also interacts with tubulin to remodel the function of CRMP2 (Brot et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Mapping CRMP3 domains involved in dendrite morphogenesis and voltage-gated calcium channel regulation

Quach

Wilson

Rogemond

et al. 2013

Journal of Cell Science

View full text Add to dashboard Cite

SummaryAlthough hippocampal neurons are well-distinguished by the morphological characteristics of their dendrites and their structural plasticity, the mechanisms involved in regulating their neurite initiation, dendrite growth, network formation and remodeling are still largely unknown, in part because the key molecules involved remain elusive. Identifying new dendrite-active cues could uncover unknown molecular mechanisms that would add significant understanding to the field and possibly lead to the development of novel neuroprotective therapy because these neurons are impaired in many neuropsychiatric disorders. In our previous studies, we deleted the gene encoding CRMP3 in mice and identified the protein as a new endogenous signaling molecule that shapes diverse features of the hippocampal pyramidal dendrites without affecting axon morphology. We also found that CRMP3 protects dendrites against dystrophy induced by prion peptide PrP . Here, we report that CRMP3 has a profound influence on neurite initiation and dendrite growth of hippocampal neurons in vitro. Our deletional mapping revealed that the C-terminus of CRMP3 probably harbors its dendritogenic capacity and supports an active transport mechanism. By contrast, overexpression of the C-terminal truncated CRMP3 phenocopied the effect of CRMP3 gene deletion with inhibition of neurite initiation or decrease in dendrite complexity, depending on the stage of cell development. In addition, this mutant inhibited the activity of CRMP3, in a similar manner to siRNA. Voltage-gated calcium channel inhibitors prevented CRMP3-induced dendritic growth and somatic Ca 2+ influx in CRMP3-overexpressing neurons was augmented largely via L-type channels. These results support a link between CRMP3-mediated Ca 2+ influx and CRMP3-mediated dendritic growth in hippocampal neurons.

show abstract

Critical Role of Collapsin Response Mediator Protein-associated Molecule CRAM for Filopodia and Growth Cone Development in Neurons

Cited by 47 publications

References 31 publications

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Mapping CRMP3 domains involved in dendrite morphogenesis and voltage-gated calcium channel regulation

Contact Info

Product

Resources

About