DCX in PC12 cells: CREB-mediated transcription and neurite outgrowth

Shmueli, Orit; Gdalyahu, Amos; Sorokina, K. N.; Nevo, Eviater; Avivi, Aaron; Reiner, Orly

doi:10.1093/hmg/10.10.1061

Cited by 33 publications

(20 citation statements)

References 58 publications

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“…Taken together with the findings in previous reports, our data strongly suggest that PACAP-induced PKA activation results in the release of DCX from microtubules and that this released DCX associates with actin filaments through neurabin2 at the growth cone. cAMP-dependent neurite extension and axon formation are well known (52,53), but the detailed mechanism remains unclear. The PKA-regulated switching mechanism of DCX function between microtubules and actin filaments may be involved in neuronal migration and morphological change in response to extracellular cues.…”

Section: Discussionmentioning

confidence: 99%

Phosphorylation of Doublecortin by Protein Kinase A Orchestrates Microtubule and Actin Dynamics to Promote Neuronal Progenitor Cell Migration

Toriyama¹,

Mizuno²,

Fukami

et al. 2012

Journal of Biological Chemistry

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Background: Regulation of neuronal progenitor cell migration is critical for proper brain lamination. Results: G protein-coupled receptor signaling promotes cell migration, lamellipodium formation, and Rac activation by phosphorylating a microtubule-associated protein, doublecortin. Conclusion: Doublecortin is released from microtubules and induces actin reorganization in a phosphorylation-dependent manner. Significance: This is the first evidence for the coordinated regulation of microtubule and actin dynamics.

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Section: Discussionmentioning

confidence: 99%

Phosphorylation of Doublecortin by Protein Kinase A Orchestrates Microtubule and Actin Dynamics to Promote Neuronal Progenitor Cell Migration

Toriyama¹,

Mizuno²,

Fukami

et al. 2012

Journal of Biological Chemistry

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“…The result suggested that cofilin activity at axon tips is important for JIP3-enhanced axon elongation. However, many other JNK substrates, such as doublecortin (DCX), MAP2, the heavy subunit of the neurofilament protein (NFH), and superior cervical ganglia clone 10 (SCG10), have been reported to be important for neurite outgrowth (37,51,(53)(54)(55)(56). Whether these JNK substrates participate in the effect of JIP3 on axon elongation is worthy of further investigation.…”

Section: Jip3mentioning

confidence: 99%

c-Jun NH2-terminal Kinase (JNK)-interacting Protein-3 (JIP3) Regulates Neuronal Axon Elongation in a Kinesin- and JNK-dependent Manner

Sun

Zhai

et al. 2013

Journal of Biological Chemistry

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“…The S47 residue has been mutated in several lissencephaly patients, 11,12,22 and overexpression of the mutated protein (S47R) abolished neurite outgrowth in PC12 cells. 23 If we assume that each of these five phosphorylation sites can be phosphorylated in an independent manner, then there are 2 5 (or 32) different combinatorial events. Although this may be an overestimation, it leaves us with numerous possibilities to explain the complex changes occurring in a migrating neuron.…”

Section: Modes Of Radial Migrationmentioning

confidence: 99%

DCXs Phosphorylation by Not Just aNother Kinase (JNK)

et al. 2004

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The mammalian cortex is generally subdivided into six organized layers, which are formed during development in an organized fashion. This organized cortical layering is disrupted in case of mutations in the doublecortin (DCX) gene. DCX is a Microtubule Associated Protein (MAP). However, besides stabilization of microtubules, it may be involved in additional functions. The participation of this molecule in signal transduction is beginning to emerge via discovery of interacting molecules and its regulation by phosphorylation using several different kinases. We raise the hypothesis, that the combinatorial phosphorylation of DCX by different kinases and at different sites may be a molecular regulatory switch in the transition of a migrating neuron through multiple phases of migration. Our recent research has suggested the involvement of DCX in the JNK (Jun-N-terminal Kinase) pathway. The JNK pathway is linked to the reelin pathway, known to regulate cortical layering. Positioning of DCX in this signaling pathway opens up additional possibilities of understanding how migrating neurons are controlled.Neuronal positioning in the cortex is a genetically determined paradigm highly conserved among mammals. Therefore, accumulated molecular information both from human and mouse allowed initially the identification of many key players in this process, followed by the rudimentary positioning of these molecules in genetic pathways (reviewed in ref. 1). One of the major challenges in the field is to uncover physiologically relevant pathways that initiate at receptor activation, affect intracellular signal transduction, and are translated to neuronal movement coupled with target recognition and circuit formation. MODES OF RADIAL MIGRATIONThe advent of time-lapse imaging has changed our view regarding how cortical neurons migrate radially. Previous studies have pointed to the fact that neurons migrating along radial glia have a distinct morphology, with a growth-cone-like structure frequently present at the end of the leading process. [2][3][4][5] Time-lapse studies have indicated that each migrating neuron undergoes a series of cellular morphology changes, 5-7 (reviewed in refs. 8,9). More specifically three different modes of movement have been defined: somal translocation, cellular locomotion, 5 and a multipolar mode. 7 Somal translocation is defined by the translocation of the entire cell body. The leading process is frequently branched, with retractions following pauses. In case of cellular locomotion, the cells have a distinct morphology resembling features of glial-guided migrating neurons. The former is the prevalent form of radial movement of the early-born cortical neurons, while the latter is adopted by those generated later in corticogenesis (reviewed in ref. 10). The third mode of multipolar radial migration is quite different from the other two. These multipolar neurons extend numerous thin processes in various directions independently of the radial glial fibers. They do not exhibit fixed cell polarity, and ...

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DCX in PC12 cells: CREB-mediated transcription and neurite outgrowth

Cited by 33 publications

References 58 publications

Phosphorylation of Doublecortin by Protein Kinase A Orchestrates Microtubule and Actin Dynamics to Promote Neuronal Progenitor Cell Migration

Phosphorylation of Doublecortin by Protein Kinase A Orchestrates Microtubule and Actin Dynamics to Promote Neuronal Progenitor Cell Migration

c-Jun NH2-terminal Kinase (JNK)-interacting Protein-3 (JIP3) Regulates Neuronal Axon Elongation in a Kinesin- and JNK-dependent Manner

DCXs Phosphorylation by Not Just aNother Kinase (JNK)

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