Olig bHLH proteins interact with homeodomain proteins to regulate cell fate acquisition in progenitors of the ventral neural tube

Previous studies have demonstrated that the neural tube/notochord complex is required for skeletal muscle development within somites. In order to explore the localization of myogenic inducing signals within the neural tube, dorsal or ventral neural tube halves were cultured in contact with single somites or pieces of segmental plate mesoderm. Somites and segmental plates cultured with the dorsal half of the neural tube exhibited 70% and 85% myogenic response rates, as determined by immunostaining for myosin heavy chain. This response was slightly lower than the 100% response to whole neural tube/notochord, but was much greater than the 30% and 10% myogenic response to ventral neural tube with and without notochord. These results demonstrate that the dorsal neural tube emits a potent myogenic inducing signal which accounts for most of the inductive activity of whole neural tube/notochord. However, a role for ventral neural tube/notochord in somite myogenic induction was clearly evident from the larger number of myogenic cells induced when both dorsal neural tube and ventral neural tube/notochord were present. To address the role of a specific dorsal neural tube factor in somite myogenic induction, we tested the ability of Wnt-1-expressing fibroblasts to promote paraxial mesoderm myogenesis in vitro. We found that cells expressing Wnt-1 induced a small number of somite and segmental plate cells to undergo myogenesis. This finding is consistent with the localized dorsal neural tube inductive activity described above, but since the ventral neural tube/notochord also possesses myogenic inductive capacity yet does not express Wnt-1, additional inductive factors are likely involved.

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Cell-autonomous shift from axial to paraxial mesodermal development in zebrafish floating head mutants

Development ◽

10.1242/dev.121.12.4257 ◽

1995 ◽

Vol 121 (12) ◽

pp. 4257-4264 ◽

Cited By ~ 25

Author(s):

M.E. Halpern ◽

C. Thisse ◽

R.K. Ho ◽

B. Thisse ◽

B. Riggleman ◽

...

Keyword(s):

Neural Tube ◽

Single Cells ◽

Floor Plate ◽

Paraxial Mesoderm ◽

Wild Type ◽

Genetic Mosaics ◽

Essential Step ◽

Ventral Neural Tube ◽

Mesodermal Development

Zebrafish floating head mutant embryos lack notochord and develop somitic muscle in its place. This may result from incorrect specification of the notochord domain at gastrulation, or from respecification of notochord progenitors to form muscle. In genetic mosaics, floating head acts cell autonomously. Transplanted wild-type cells differentiate into notochord in mutant hosts; however, cells from floating head mutant donors produce muscle rather than notochord in wild-type hosts. Consistent with respecification, markers of axial mesoderm are initially expressed in floating head mutant gastrulas, but expression does not persist. Axial cells also inappropriately express markers of paraxial mesoderm. Thus, single cells in the mutant midline transiently co-express genes that are normally specific to either axial or paraxial mesoderm. Since floating head mutants produce some floor plate in the ventral neural tube, midline mesoderm may also retain early signaling capabilities. Our results suggest that wild-type floating head provides an essential step in maintaining, rather than initiating, development of notochord-forming axial mesoderm.

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The zebrafish T-box genesno tailandspadetailare required for development of trunk and tail mesoderm and medial floor plate

Development ◽

10.1242/dev.129.14.3311 ◽

2002 ◽

Vol 129 (14) ◽

pp. 3311-3323 ◽

Cited By ~ 6

Author(s):

Sharon L. Amacher ◽

Bruce W. Draper ◽

Brian R. Summers ◽

Charles B. Kimmel

Keyword(s):

Embryonic Development ◽

Neural Tube ◽

Transcriptional Regulators ◽

Floor Plate ◽

Wild Type ◽

T Box ◽

No Tail ◽

Ventral Neural Tube ◽

Plate Formation ◽

In Cells

T-box genes encode transcriptional regulators that control many aspects of embryonic development. Here, we demonstrate that the mesodermally expressed zebrafish spadetail (spt)/VegT and no tail (ntl)/Brachyury T-box genes are semi-redundantly and cell-autonomously required for formation of all trunk and tail mesoderm. Despite the lack of posterior mesoderm in spt–;ntl– embryos, dorsal-ventral neural tube patterning is relatively normal, with the notable exception that posterior medial floor plate is completely absent. This contrasts sharply with observations in single mutants, as mutations singly in ntl or spt enhance posterior medial floor plate development. We find that ntl function is required to repress medial floor plate and promote notochord fate in cells of the wild-type notochord domain and that spt and ntl together are required non cell-autonomously for medial floor plate formation, suggesting that an inducing signal present in wild-type mesoderm is lacking in spt–;ntl– embryos.

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A singularity of PDGF alpha-receptor expression in the dorsoventral axis of the neural tube may define the origin of the oligodendrocyte lineage

Development ◽

10.1242/dev.117.2.525 ◽

1993 ◽

Vol 117 (2) ◽

pp. 525-533 ◽

Cited By ~ 35

Author(s):

N.P. Pringle ◽

W.D. Richardson

Keyword(s):

Spinal Cord ◽

Cell Fate ◽

Neural Tube ◽

Ventricular Zone ◽

Central Canal ◽

Receptor Expression ◽

Foramen Of Monro ◽

Dorsoventral Axis ◽

Germinal Zone ◽

Restricted Region

During rat embryogenesis, PDGF alpha receptor (PDGF-alpha R) mRNA is expressed in the ventral half of the spinal cord in two longitudinal columns, one each side of the central canal. Initially, these columns are only two cells wide but the cells subsequently appear to proliferate and disseminate throughout the spinal cord. Our previous studies of PDGF-alpha R expression in the developing CNS suggested that PDGF-alpha R may be a useful marker of the oligodendrocyte lineage in situ. The data presented here complement those studies and lead us to propose that the earliest oligodendrocyte precursors in the spinal cord originate in a very restricted region of the ventricular zone during a brief window of time around embryonic day 14 (E14). In the embryonic brain, migrating PDGF-alpha R+ cells appear to originate in a localized germinal zone in the ventral diencephalon (beneath the foramen of Monro). Our data demonstrate that gene expression and cell fate can be regulated with exquisite spatial resolution along the dorsoventral axis of the mammalian neural tube.

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Direct action of the nodal-related signal cyclops in induction of sonic hedgehog in the ventral midline of the CNS

Development ◽

10.1242/dev.127.18.3889 ◽

2000 ◽

Vol 127 (18) ◽

pp. 3889-3897 ◽

Cited By ~ 4

Author(s):

F. Muller ◽

S. Albert ◽

P. Blader ◽

N. Fischer ◽

M. Hallonet ◽

...

Keyword(s):

Sonic Hedgehog ◽

Neural Tube ◽

Direct Action ◽

Brain Regions ◽

Floor Plate ◽

Ventral Midline ◽

Signal Transducers ◽

Step Model ◽

Ventral Neural Tube ◽

Differential Responsiveness

The secreted molecule Sonic hedgehog (Shh) is crucial for floor plate and ventral brain development in amniote embryos. In zebrafish, mutations in cyclops (cyc), a gene that encodes a distinct signal related to the TGF(beta) family member Nodal, result in neural tube defects similar to those of shh null mice. cyc mutant embryos display cyclopia and lack floor plate and ventral brain regions, suggesting a role for Cyc in specification of these structures. cyc mutants express shh in the notochord but lack expression of shh in the ventral brain. Here we show that Cyc signalling can act directly on shh expression in neural tissue. Modulation of the Cyc signalling pathway by constitutive activation or inhibition of Smad2 leads to altered shh expression in zebrafish embryos. Ectopic activation of the shh promoter occurs in response to expression of Cyc signal transducers in the chick neural tube. Furthermore an enhancer of the shh gene, which controls ventral neural tube expression, is responsive to Cyc signal transducers. Our data imply that the Nodal related signal Cyc induces shh expression in the ventral neural tube. Based on the differential responsiveness of shh and other neural tube specific genes to Hedgehog and Cyc signalling, a two-step model for the establishment of the ventral midline of the CNS is proposed.

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Pcgf1 regulates early neural tube development through histone methylation in zebrafish

10.21203/rs.3.rs-25978/v1 ◽

2020 ◽

Author(s):

Xinyue Li ◽

Guangyu Ji ◽

Juan Zhou ◽

Jingyi Du ◽

Xian Li ◽

...

Keyword(s):

Cell Fate ◽

Neural Tube ◽

Histone Methylation ◽

Control Cell ◽

Neural Induction ◽

Induction Phase ◽

Zebrafish Embryos ◽

Rna Seq ◽

Self Renewal ◽

Neural Tube Development

Abstract Objective Early neural tube development in the embryo includes neural induction and self-renewal of neural stem cells (NSCs). The abnormal of neural tube development could lead to neural tube defects. The research on the mechanism of neural induction is the key to reveal the pathogenesis of the abnormal of neural tube. Though studies have confirmed a genetic component, the responsible mechanisms for the abnormal of neural tube are still largely unknown. Polycomb repressive complex 1 (PRC1) plays an important role in regulating early embryonic development, and has been sub-classified into six major complexes based on the presence of a Pcgf subunit. Pcgf1, as one of six Pcgf paralogs, is an important requirement in early embryonic brain development. Here, we intended to investigate the role and mechanism of Pcgf1 in early neural tube development of zebrafish embryos. Material and methods Morpholino (MO) antisense oligonucleotides were used to construct a Pcgf1 loss-of function zebrafish model. We analyzed the phenotype of zebrafish embryos and the expression of related genes in the process of neural induction by in situ hybridization, immunolabelling and RNA-sEq. The regulation of histone modifications on gene was detected by western blot and chromatin immunoprecipitation. Results In this study, we found that zebrafish embryos exhibited small head and reduced or even absence of telencephalon after inhibiting the expression of Pcgf1. Moreover, the neural induction process of zebrafish embryos was abnormal, and the subsequent NSCs self-renewal was inhibited under the inhibition of Pcgf1. RNA-seq and gene ontology (GO) analysis identified that the differentially expressed genes were enriched in many functional categories which related to the development phenotype. Finally, our results showed that Pcgf1 regulated the trimethylation of histone H3K27 in the Ngn1 and Otx2 promoter regions, and the levels of H3K4me3 at the promoters of Pou5f3 and Nanog. Conclusion Together, our data for the first time demonstrate that Pcgf1 plays an essential role in early neural induction phase through histone methylation in neural tube development. Our findings reveal a critical context-specific function for Pcgf1 in directing PRC1 to control cell fate.

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