Reverse Signaling via a Glycosyl-Phosphatidylinositol-Linked Ephrin Prevents Midline Crossing by Migratory Neurons during Embryonic Development in<i>Manduca</i>

Coate, Thomas M.; Wirz, J; Copenhaver, Philip F.

doi:10.1523/jneurosci.5691-07.2008

Cited by 11 publications

(33 citation statements)

References 68 publications

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“…1A), regulated by attractive and repulsive guidance cues encountered by the motile cells during different phases of their differentiation (Copenhaver and Taghert, 1989b;Copenhaver, 1993;Wright et al, 1999;Coate et al, 2008). Between 30 and 40 hpf, a packet of ϳ300 neurons (EP cells) delaminates from a neurogenic placode in the dorsal foregut, coincident with their terminal mitoses (Copenhaver and Taghert, 1990).…”

Section: Resultsmentioning

confidence: 99%

“…Average values were calculated from replicate groups of embryos (N Ն 10 per condition), and each experiment was repeated Ն3 times. To measure ectopic growth by the EP cells, both the number of neurons and the cumulative distance of neurites that had traveled onto the interband muscles (between band pathways) were determined from camera lucida images, as previously described (Coate et al, 2008;Ramaker et al, 2013). The extent of ectopic outgrowth was normalized to the diameter of the midgut in each preparation to compensate for any distortions caused by our fixation and immunohistochemical staining methods (typically this distortion was Ͻ10% of the average midgut diameters in each experiment).…”

Section: Methodsmentioning

confidence: 99%

“…A small incision was made in the dorsal body wall of embryos placed in culture (at 53 hpf), and MOs were delivered into the EP cells with 0.6 -1% Endo-Porter (Gene Tools), as previously described (Coate et al, 2008). Based on our past studies, we estimate that this method results in a 10-fold dilution of the MOs, whereby the EP cells were exposed to a final concentration of ϳ10 M. Control embryos were treated with equivalent concentrations of standard control MOs plus Endo-Porter.…”

Section: Methodsmentioning

confidence: 99%

“…For binding assays using MsCont-Fc fusion constructs, dissected embryos were fixed with 4% PFA, permeabilized briefly with PBS plus 0.1% Triton X-100, and then incubated for 2 h with 400 g/ml MsCont-Fc in defined saline. Matched sets of preparations were treated (1) with medium alone, (2) with ChromPur human IgG Fc fragments (Jackson ImmunoResearch, #009-000-008); or (3) with a variety of control Fc fusion proteins, including MsEph-Fc and MsEphrin-Fc (Coate et al, 2008). The embryos were subsequently postfixed with PFA for 30 -60 min.…”

Section: Methodsmentioning

confidence: 99%

“…2B) or a variety of control MOs for 24 h, spanning the periods of EP cell migration and outgrowth. The embryos were subsequently fixed and immunostained with anti-pan-Fas II antibodies to fully label the neurons, glial cells, and their processes, which we could readily distinguish by their morphologies and positions using our camera lucida-based methods (Wright et al, 1999;Coate et al, 2008).…”

Section: Glial Contactin Is Required For Preventing Ectopic Neuronal mentioning

confidence: 99%

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Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration

Ramaker

Swanson²,

Copenhaver

2016

J. Neurosci.

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Amyloid precursor protein (APP) was originally identified as the source of ␤-amyloid peptides that accumulate in Alzheimer's disease (AD), but it also has been implicated in the control of multiple aspects of neuronal motility. APP belongs to an evolutionarily conserved family of transmembrane proteins that can interact with a variety of adapter and signaling molecules. Recently, we showed that both APP and its insect ortholog [APPL (APP-Like)] directly bind the heterotrimeric G-protein Go␣, supporting the model that APP can function as an unconventional Go␣-coupled receptor. We also adapted a well characterized assay of neuronal migration in the hawkmoth, Manduca sexta, to show that APPL-Go␣ signaling restricts ectopic growth within the developing nervous system, analogous to the role postulated for APP family proteins in controlling migration within the mammalian cortex. Using this assay, we have now identified Manduca Contactin (MsContactin) as an endogenous ligand for APPL, consistent with previous work showing that Contactins interact with APP family proteins in other systems. Using antisense-based knockdown protocols and fusion proteins targeting both proteins, we have shown that MsContactin is selectively expressed by glial cells that ensheath the migratory neurons (expressing APPL), and that MsContactin-APPL interactions normally prevent inappropriate migration and outgrowth. These results provide new evidence thatContactins can function as authentic ligands for APP family proteins that regulate APP-dependent responses in the developing nervous system. They also support the model that misregulated Contactin-APP interactions might provoke aberrant activation of Go␣ and its effectors, thereby contributing to the neurodegenerative sequelae that typify AD.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Glial Contactin Is Required For Preventing Ectopic Neuronal mentioning

confidence: 99%

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Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration

Ramaker

Swanson²,

Copenhaver

2016

J. Neurosci.

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Ephrin-A1 Regulates Cell Remodeling and Migration

et al. 2011

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The Eph family of receptor tyrosine kinases and their cognate ligands, the Ephrins, form a coordinated program of cell contact-mediated migration control, polarity establishment, and tissue architecture development. Specifically, the ligand Ephrin-A1 has been shown to regulate cell morphology and motility through the activation of EphA receptors, which signal to the PI3K pathway to induce cell retraction. MEFs with PI3K subunit p85b knockout (p85b À/À ) exhibited markedly reduced cell retraction following Ephrin-A1 stimulation. Ephrin-A1 also serves as an inhibitory substrate for cell spreading and migration. Moreover, Ephrin-A1 treatment results in the dephosphorylation of paxillin and induces the reorganization of phosphopaxillin-containing focal adhesions. The Ephrin-A1 regulated paxillin dephosphorylation is phosphatase dependent, but p85b independent. The present study serves to demonstrate a novel molecular signaling pathways that regulate Ephrin-A1-regulated cell retraction and interaction to the substrate.

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Ephrin-B2/EphA4 forward signaling is required for regulation of radial migration of cortical neurons in the mouse

Yan

Jiang

et al. 2014

Neurosci. Bull.

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Postmitotic neurons in the neocortex migrate to appropriate positions and form layered structures of nascent cortex during brain development. The migration of these neurons requires precise control and coordination of a large number of molecules such as axon guidance cues. The Eph-ephrin signaling pathway plays important roles in the development of the nervous system in a wide variety of ways, including cell segregation, axon pathfinding, and neuron migration. However, the role of ephrin-B2/EphA4 signaling in cortical neuron migration remains elusive. Here we demonstrated that ephrin-B2 and its receptor EphA4 were expressed in complementary and overlapping patterns in the developing neocortex. Deletion of the EphA4 gene in the embryonic cerebral cortex resulted in faster migration of cortical neurons, whereas knockdown or overexpression of ephrin-B2 did not alter the normal process of migration. These results suggest that ephrin-B2 forward signaling through EphA4 is required for the precise control of cortical neuron migration.

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Reverse Signaling via a Glycosyl-Phosphatidylinositol-Linked Ephrin Prevents Midline Crossing by Migratory Neurons during Embryonic Development inManduca

Cited by 11 publications

References 68 publications

Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration

Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration

Ephrin-A1 Regulates Cell Remodeling and Migration

Ephrin-B2/EphA4 forward signaling is required for regulation of radial migration of cortical neurons in the mouse

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