High efficiency gene transfer into the embryonic chicken CNS using B‐subgroup retroviruses

Homburger, Sheila A.; Fekete, Donna M.

doi:10.1002/(sici)1097-0177(199605)206:1<112::aid-aja10>3.3.co;2-h

Cited by 11 publications

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“…3K). As it takes about 15 to 18 hours after infection to achieve high levels o f ectopic protein expression (26), the time o f competence to convert ectodenn to neural crest appears to decline b y HH stage 11 (13 to 14 tions performed between HH stages 5 and 11 somite stage).…”

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confidence: 99%

Neural Crest Specification Regulated by the Helix-Loop-Helix Repressor Id2

Martinsen

Bronner‐Fraser

1998

Science

133

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Vertebrate neural crest cells, derived from the neural folds, generate a variety of tissues, such as cartilage, ganglia, and cranial (intramembranous) bone. The chick homolog of the helix-loop-helix transcriptional regulator Id2 is expressed in cranial but not trunk neural folds and subsequently in some migrating cranial neural crest cells. Ectopic expression of Id2 with recombinant retroviruses converted ectodermal cells to a neural crest fate, demonstrating that proper regulation of Id2 is important for sustaining epidermal traits. In addition, overexpression of Id2 resulted in overgrowth and premature neurogenesis of the dorsal neural tube. These results suggest that Id2 may allocate ectodermal precursors into neural rather than epidermal lineages.

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confidence: 99%

Neural Crest Specification Regulated by the Helix-Loop-Helix Repressor Id2

Martinsen

Bronner‐Fraser

1998

Science

133

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“…The majority of hair cells and supporting cells withdraw from the cell cycle between E5 and E7 in the middle regions of the BP and the entire organ is largely quiescent by E8.5 (Katayama and Corwin, 1989). Because virus-mediated protein expression is detectable within 10h and is robust by 24h after virus injection (Homburger and Fekete, 1996), we expect that many infected sensory cells will begin to express the Vangl2 transgene while they are still mitotic. Infected cells will continue to express the transgene after they differentiate.…”

Section: Resultsmentioning

confidence: 99%

Non-cell-autonomous planar cell polarity propagation in the auditory sensory epithelium of vertebrates

Sienknecht

Anderson

Parodi

et al. 2011

Developmental Biology

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Sensory epithelia of the inner ear require a coordinated alignment of hair cell stereociliary bundles as an essential element of mechanoreceptive function. Hair cell bundle alignment is mediated by core planar cell polarity (PCP) proteins, such as Vangl2, that localize asymmetrically to the circumference of the cell near its apical surface. During early phases of cell orientation in the chicken basilar papilla (BP), Vangl2 is present at supporting cell junctions that lie orthogonal to the polarity axis. Several days later, there is a striking shift in the Vangl2 pattern associated with hair cells that reorient toward the distal (apical) end of the organ. How the localization of PCP proteins transmits planar polarity information across the developing sensory epithelium remains unclear. To address this question, the normal asymmetric localization of Vangl2 was disrupted by overexpressing Vangl2 in clusters of cells. The BP was infected with replication-competent retrovirus encoding Vangl2 prior to hair cell differentiation. Virus-infected cells showed normal development of individual stereociliary bundles, indicating that asymmetry was established at the cellular level. Yet, bundles were misoriented in ears infected with Vangl2 virus but not Wnt5a virus. Notably, Vangl2 misexpression did not randomize bundle orientations but rather generated larger variations around a normal mean angle. Cell clusters with excess Vangl2 could induce non-autonomous polarity disruptions in wildtype neighboring cells. Furthermore, there appears to be a directional bias in the propagation of bundle misorientation that is towards the abneural edge of the epithelium. Finally, regional bundle reorientation was inhibited by Vangl2 overexpression. In conclusion, ectopic Vangl2 protein causes inaccurate local propagation of polarity information, and Vangl2 acts in a non-cell-autonomous fashion in the sensory system of vertebrates.

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“…β-cat::S-SCAM-dn was previously shown to selectively block β-catenin interactions with S-SCAM (Nishimura et al, 2002). The dominant negative cDNA constructs were subcloned separately into the avian-specific retroviral vector RCASBP (B envelope subgroup type; (Homburger and Fekete, 1996). RCASBP containing GFP cDNA was a gift of Dr. Constance Cepko (Harvard Medical School, Boston, MA).…”

Section: Methodsmentioning

confidence: 99%

The Postsynaptic Adenomatous Polyposis Coli (APC) Multiprotein Complex Is Required for Localizing Neuroligin and Neurexin to Neuronal Nicotinic Synapsesin Vivo

Rosenberg

Yang²,

Mohn³

et al. 2010

J. Neurosci.

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Synaptic efficacy requires that presynaptic and postsynaptic specializations align precisely and mature coordinately. The underlying mechanisms are poorly understood, however. We propose that adenomatous polyposis coli protein (APC) is a key coordinator of presynaptic and postsynaptic maturation. APC organizes a multiprotein complex that directs nicotinic acetylcholine receptor (nAChR) localization at postsynaptic sites in avian ciliary ganglion neurons in vivo. We hypothesize that the APC complex also provides retrograde signals that direct presynaptic active zones to develop in register with postsynaptic nAChR clusters. In our model, the APC complex provides retrograde signals via postsynaptic neuroligin that interacts extracellularly with presynaptic neurexin. S-SCAM (synaptic cell adhesion molecule) and PSD-93 (postsynaptic density-93) are scaffold proteins that bind to neuroligin. We identify S-SCAM as a novel component of neuronal nicotinic synapses. We show that S-SCAM, PSD-93, neuroligin and neurexin are enriched at ␣3*-nAChR synapses. PSD-93 and S-SCAM bind to APC and its binding partner ␤-catenin, respectively. Blockade of selected APC and ␤-catenin interactions, in vivo, leads to decreased postsynaptic accumulation of S-SCAM, but not PSD-93. Importantly, neuroligin synaptic clusters are also decreased. On the presynaptic side, there are decreases in neurexin and active zone proteins. Further, presynaptic terminals are less mature structurally and functionally. We define a novel neural role for APC by showing that the postsynaptic APC multiprotein complex is required for anchoring neuroligin and neurexin at neuronal synapses in vivo. APC human gene mutations correlate with autism spectrum disorders, providing strong support for the importance of the association, demonstrated here, between APC, neuroligin and neurexin.

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High efficiency gene transfer into the embryonic chicken CNS using B‐subgroup retroviruses

Cited by 11 publications

References 0 publications

Neural Crest Specification Regulated by the Helix-Loop-Helix Repressor Id2

Neural Crest Specification Regulated by the Helix-Loop-Helix Repressor Id2

Non-cell-autonomous planar cell polarity propagation in the auditory sensory epithelium of vertebrates

The Postsynaptic Adenomatous Polyposis Coli (APC) Multiprotein Complex Is Required for Localizing Neuroligin and Neurexin to Neuronal Nicotinic Synapsesin Vivo

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