Disabled-1-Regulated Adhesion of Migrating Neurons to Radial Glial Fiber Contributes to Neuronal Positioning during Early Corticogenesis

Sanada, Kamon; Gupta, Amitabh; Tsai, Li‐Huei

doi:10.1016/s0896-6273(04)00222-3

Cited by 152 publications

(156 citation statements)

References 47 publications

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“…Five days later, at E19.5, Dab1 shRNA neurons were significantly deeper than matched vector controls (P = 0.011) (Fig. 8A,B,D), as expected (Hammond et al 2001;Tabata and Nakajima 2002;Sanada et al 2004;Olson et al 2006). Dab1 shRNA neurons were also slightly deeper than controls at E17.5 (data not shown).…”

Section: Dab1 Role In Cul5-regulated Neuron Positioningsupporting

confidence: 69%

“…In addition, in utero electroporation of Dab1 shRNA at E18 caused neurons to lag behind their siblings, and their leading processes were less developed (Olson et al 2006). In utero infection of wild-type or Dab1 mutant brains with retroviruses encoding phosphorylation site mutants of Dab1 allowed the role of Dab1 phosphorylation in the movement of individual neurons to be tested (Sanada et al 2004). Dab1 mutants that were unable to rescue movement were found deeper in the cortical plate and were closer to their radial glia guides than control neurons.…”

Section: Dab1 Role In Cul5-regulated Neuron Positioningmentioning

confidence: 99%

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Cullin 5 regulates Dab1 protein levels and neuron positioning during cortical development

Li¹,

Allen²,

Simó³

et al. 2007

Genes Dev.

130

138

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Section: Dab1 Role In Cul5-regulated Neuron Positioningsupporting

confidence: 69%

Section: Dab1 Role In Cul5-regulated Neuron Positioningmentioning

confidence: 99%

Cullin 5 regulates Dab1 protein levels and neuron positioning during cortical development

Li¹,

Allen²,

Simó³

et al. 2007

Genes Dev.

130

138

View full text Add to dashboard Cite

show abstract

“…The distinction between radial and tangential migration may be blurred somewhat in the RMS, as neurons undergo chain migration but through a substrate of glial guidance. A similar requirement for LIS1 and components of the reelin pathway in both radial and tangential migration have reported 18,[60][61][62] .…”

Section: As a Regulator Of Radial And Tangential Migrationsupporting

confidence: 65%

Doublecortin maintains bipolar shape and nuclear translocation during migration in the adult forebrain

et al. 2006

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The ability of the mature mammalian nervous system to continually produce neuronal precursors is of considerable importance, as manipulation of this process might one day permit the replacement of cells lost as a result of injury or disease. In mammals, the anterior subventricular zone (SVZa) region is one of the primary sites of adult neurogenesis. Here we show that Doublecortin (DCX), a widely used marker for newly generated neurons, when deleted in mouse results in a severe morphological defect in the rostral migratory stream and delayed neuronal migration that is independent of direction or responsiveness to Slit chemorepulsion. DCX is required for nuclear translocation and maintenance of bipolar morphology during migration of these cells. Our data identifies a critical function for DCX in the movement of newly generated neurons in the adult brain.In the rodent and primate brain, the anterior region of the lateral ventricle and the hippocampus are the primary sites of adult neurogenesis [1][2][3][4][5][6][7] . These neuroblasts, upon completing migration, are capable of maturing into fully differentiated neurons, integrating into local synaptic circuits and may be important in adult cognitive processing [8][9][10][11] .The mechanisms controlling the targeted translocation of large numbers of cells to the olfactory bulb (OB) over a considerable distance (>5 mm in the adult mouse) are an issue of intense investigation. These neurons translocate using a process known as chain migration, whereby the cells use each other as the migratory substrate 12 . These newly generated neurons are derived from SVZa glial fibrillary acidic protein (GFAP)-positive astrocytes 13,14 , which also ensheath them as they move through extensive interconnected networks along the lining of the lateral ventricle in the rostral forebrain and the rostral migratory stream (RMS) 15 . There, they are under the control of extracellular migration guidance cues, including the secreted ligands Slit and Reelin [16][17][18][19] , the receptors ErbB4 and Deleted in Colorectal Carcinoma (DCC) 20,21 , as well as integrins and neural cell adhesion molecule [21][22][23] . Upon reaching the bulb, the neurons turn and migrate in a radial direction 24 , integrating into either the granule cell layer or the periglomerular network 25 . 3The X-linked gene doublecortin (DCX) is mutated in some patients with the severe neuronal migration defect called classical lissencephaly or double cortex syndrome 26,27 . This migration defect is likely to be cell autonomous, because in females with a heterozygous mutation, approximately half of the neurons are misplaced within the cerebral cortex as would be expected from random X-chromosome inactivation. As a result, males display a four-layered agyric cortex and females display a subcortical band of heterotopic neurons. It was surprising, therefore, that the Dcx knockout mice displayed no appreciable defect in cortical neuronal lamination or positioning 28 . One possible explanation for these species differences ...

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“…3D ; compare lanes 4-6). For neuronal migration, Tyr-phosphorylated DAB1 (pY-DAB1) is essential, because it is compromised by expression of the "5YF" DAB1 mutant, in which fi ve Tyr residues are replaced with Phe, a structurally similar but nonphosphorylatable aa ( 8 ). In the RKO cells expressing 5YF-DAB1, we found that the pY-ABL1b level remained low ( Fig.…”

Section: Research Articlementioning

confidence: 90%

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

et al. 2015

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We have recently identifi ed a metastasis suppressor gene for colorectal cancer: AES / Aes , which encodes an endogenous inhibitor of NOTCH signaling. When Aes is knocked out in the adenomatous epithelium of intestinal polyposis mice, their tumors become malignant, showing marked submucosal invasion and intravasation. Here, we show that one of the genes induced by NOTCH signaling in colorectal cancer is DAB1 / Dab1 . Genetic depletion of DAB1 suppresses cancer invasion and metastasis in the NOTCH signaling-activated mice. DAB1 is phosphorylated by ABL tyrosine kinase, which activates ABL reciprocally. Consistently, inhibition of ABL suppresses cancer invasion in mice. Furthermore, we show that one of the targets of ABL is the RAC/RHOGEF protein TRIO, and that phosphorylation at its Tyr residue 2681 (pY2681) causes RHO activation in colorectal cancer cells. Its unphosphorylatable mutation TRIO Y2681F reduces RHOGEF activity and inhibits invasion of colorectal cancer cells. Importantly, TRIO pY2681 correlates with signifi cantly poorer prognosis of patients with colorectal cancer after surgery. SIGNIFICANCE:These results indicate that TRIO pY2681 is one of the downstream effectors of NOTCH signaling activation in colorectal cancer, and can be a prognostic marker, helping to determine the therapeutic modality of patients with colorectal cancer. Cancer Discov; 5(2);[198][199][200][201][202][203][204][205][206][207][208][209][210][211]

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Disabled-1-Regulated Adhesion of Migrating Neurons to Radial Glial Fiber Contributes to Neuronal Positioning during Early Corticogenesis

Cited by 152 publications

References 47 publications

Cullin 5 regulates Dab1 protein levels and neuron positioning during cortical development

Cullin 5 regulates Dab1 protein levels and neuron positioning during cortical development

Doublecortin maintains bipolar shape and nuclear translocation during migration in the adult forebrain

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

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