Murine forebrain and midbrain crest cells generate different characteristic derivatives <i>in vitro</i>

Chareonvit, Suconta; Osumi, Noriko; Ikeda, Masa Aki; Eto, Kazuhiro

doi:10.1046/j.1440-169x.1997.t01-3-00011.x

Cited by 8 publications

(6 citation statements)

References 68 publications

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“…For example, works from Patrick Tam's lab [62,63] and Osumi-Yamashita's lab [64-67] clearly showed that DiI lineage tracing could be used effectively in mouse embryos in combination with whole embryo culture to study mammalian NCC development. Our labeling method utilizes a Cre-loxP/EGFP reporter system, in which labeling is both constant and continuous.…”

Section: Resultsmentioning

confidence: 99%

Novel migrating mouse neural crest cell assay system utilizing P0-Cre/EGFP fluorescent time-lapse imaging

et al. 2011

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BackgroundNeural crest cells (NCCs) are embryonic, multipotent stem cells. Their long-range and precision-guided migration is one of their most striking characteristics. We previously reported that P0-Cre/CAG-CAT-lacZ double-transgenic mice showed significant lacZ expression in tissues derived from NCCs.ResultsIn this study, by embedding a P0-Cre/CAG-CAT-EGFP embryo at E9.5 in collagen gel inside a culture glass slide, we were able to keep the embryo developing ex vivo for more than 24 hours; this development was with enough NCC fluorescent signal intensity to enable single-cell resolution analysis, with the accompanying NCC migration potential intact and with the appropriate NCC response to the extracellular signal maintained. By implantation of beads with absorbed platelet-derived growth factor-AA (PDGF-AA), we demonstrated that PDGF-AA acts as an NCC-attractant in embryos.We also performed assays with NCCs isolated from P0-Cre/CAG-CAT-EGFP embryos on culture plates. The neuromediator 5-hydroxytryptamine (5-HT) has been known to regulate NCC migration. We newly demonstrated that dopamine, in addition to 5-HT, stimulated NCC migration in vitro. Two NCC populations, with different axial levels of origins, showed unique distribution patterns regarding migration velocity and different dose-response patterns to both 5-HT and dopamine.ConclusionsAlthough avian species predominated over the other species in the NCC study, our novel system should enable us to use mice to assay many different aspects of NCCs in embryos or on culture plates, such as migration, division, differentiation, and apoptosis.

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Section: Resultsmentioning

confidence: 99%

Novel migrating mouse neural crest cell assay system utilizing P0-Cre/EGFP fluorescent time-lapse imaging

et al. 2011

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“…We examined these possibilities using cranial neural tube explants from T14 embryos (Chareonvit et al 1997). Explants devoid of surface ectoderm were cultured for 12 hours and cells that migrated from the explant were recovered and quantified.…”

Section: Resultsmentioning

confidence: 99%

A neural crest deficit in Down syndrome mice is associated with deficient mitotic response to Sonic hedgehog

Roper

VanHorn

Cain

et al. 2009

Mechanisms of Development

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Trisomy 21 results in phenotypes collectively referred to as Down syndrome (DS) including characteristic facial dysmorphology. Ts65Dn mice are trisomic for orthologs of about half of the genes found on human chromosome 21 and exhibit DS-like craniofacial abnormalities, including a small dysmorphic mandible. Quantitative analysis of neural crest (NC) progenitors of the mandible revealed a paucity of NC and a smaller first pharyngeal arch (PA1) in Ts65Dn as compared to euploid embryos. Similar effects in PA2 suggest that trisomy causes a neurocristopathy in Ts65Dn mice (and by extension, DS). Further analyses demonstrated deficits in delamination, migration, and mitosis of trisomic NC. Addition of Sonic hedgehog (Shh) growth factor to trisomic cells from PA1 increased cell number to the same level as untreated control cells. Combined with previous demonstrations of a deficit in mitogenic response to Shh by trisomic cerebellar granule cell precursors, these results implicate common cellular and molecular bases of multiple DS phenotypes.

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“…Mouse primary cranial neural crest culture technique has been reported previously (Chareonvit et al, 1997). Midbrain and anterior hindbrain regions were identified by anatomic landmarks and microdissected from E8 Swiss Webster mouse embryos with four to six somite pairs.…”

Section: Methodsmentioning

confidence: 99%

Msx2 is a repressor of chondrogenic differentiation in migratory cranial neural crest cells†

Takahashi

Nuckolls

Takahashi

et al. 2001

Developmental Dynamics

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During early mouse embryogenesis, cranial neural crest cells (CNCC) emigrate from the posterior midbrain and rhombomeres 1 and 2 of the anterior hindbrain into the first branchial arch-derived maxillary and mandibular processes and there provide cell lineages for several phenotypes, including cartilage, bone, and tooth. Here, we report that Sox9 and Msx2 were coexpressed in a subpopulation of CNCC during their migration. Because Sox9 is a transactivator of chondrogenesis, and Msx genes can act as transcriptional repressors, we hypothesized that Sox9 expression indicates the determination of CNCC-derived chondrogenic cell lineage and that Msx2 represses chondrogenic differentiation until CNCC migration is completed within the mandibular processes. To test whether Msx2 represses chondrogenesis, we designed experiments to inhibit Msx2 function in migratory CNCC in primary cultures through the expression of loss-of-function Msx2 mutants. We showed that infection of migratory CNCC with adenovirus Msx2 mutants accelerated the rate and extent of chondrogenesis, as indicated by the expression level of type II collagen and aggrecan, and the amount of alcian blue staining. Adenovirus infections did not apparently interfere with CNCC proliferation or migration. These findings suggest that an important early event in craniofacial morphogenesis is a transient expression of both Sox9 and Msx2 during emigration into the forming mandibular processes followed by restricted expression of Sox9 within CNCCderived chondroprogenitor cells. We conclude that Msx2 serves as a repressor of chondrogenic differentiation during CNCC migration.

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Murine forebrain and midbrain crest cells generate different characteristic derivatives in vitro

Cited by 8 publications

References 68 publications

Novel migrating mouse neural crest cell assay system utilizing P0-Cre/EGFP fluorescent time-lapse imaging

Novel migrating mouse neural crest cell assay system utilizing P0-Cre/EGFP fluorescent time-lapse imaging

A neural crest deficit in Down syndrome mice is associated with deficient mitotic response to Sonic hedgehog

Msx2 is a repressor of chondrogenic differentiation in migratory cranial neural crest cells†

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