Pax6 Influences the Time and Site of Origin of Glial Precursors in the Ventral Neural Tube

Sun, Tao; Pringle, Nigel; Hardy, Adrian P.; Richardson, William D.; Smith, Hazel K.

doi:10.1006/mcne.1998.0711

Cited by 98 publications

(59 citation statements)

References 49 publications

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“…Because expression of Olig1/2 in the ventral spinal neuroepithelium is both necessary and sufficient for oligodendrocyte specification in the spinal cord (Sun et al, 2001;Zhou et al, 2001;Lu et al, 2002;Zhou and Anderson, 2002;Takebayashi et al, 2002), we hypothesize that the diminished Olig2 expression in the pMN domain is directly responsible for the delayed and reduced generation of OPCs in Nkx6.1 mutant spinal cords. A similar delay of oligodendrogenesis was also observed in Pax6 mutant spinal cords (Sun et al, 1998), in which Olig2 expression is greatly reduced (Novitch et al, 2001;Mizuguchi et al, 2001).…”

Section: Discussionsupporting

confidence: 67%

“…In the developing rodent spinal cord, expression of early oligodendrocyte marker genes, such as Olig2, Pdgfra and Sox10, is initially detected in the motoneuron precursor domain (pMN) of the ventral neuroepithelium (Sun et al, 1998;Lu et al, 2000;Zhou et al, 2000;Fu et al, 2002). Thus, it is thought that motoneurons and oligodendrocytes are sequentially generated from the same precursor cells at different time windows, with motoneurons being generated first followed by oligodendrocyte production (Richardson et al, 1997;Richardson et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Recent genetic studies have revealed that these transcription factors play important roles in controlling the development of both motoneurons and oligodendrocytes. For example, misexpression of both Olig2 and Pax6 genes can cause aberrant development of motoneurons and oligodendrocytes (Ericson et al, 1997;Sun et al, 1998;Sun et al, 2001;Zhou et al, 2001;Lu et al, 2002;Takebayashi et al, 2002;Zhou and Anderson, 2002). Nkx6.1 also has an instructive role in controlling motoneuron specification, as overexpression of the Nkx6.1 homeodomain protein induces ectopic motoneuron formation in embryonic chicken spinal cord (Briscoe et al, 2000) and mutation of Nkx6.1 leads to a drastic reduction of motoneuron genesis (Sander et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Region-specific and stage-dependent regulation of Olig gene expression and oligodendrogenesis byNkx6.1homeodomain transcription factor

Liu

Cai

et al. 2003

Development

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During early neural development, the Nkx6.1 homeodomain neural progenitor gene is specifically expressed in the ventral neural tube, and its activity is required for motoneuron generation in the spinal cord. We report that Nkx6.1 also controls oligodendrocyte development in the developing spinal cord, possibly by regulating Olig gene expression in the ventral neuroepithelium. In Nkx6.1 mutant spinal cords, expression of Olig2 in the motoneuron progenitor domain is diminished, and the generation and differentiation of oligodendrocytes are significantly delayed and reduced. The regulation of Olig gene expression by Nkx6.1 is stage dependent, as ectopic expression of Nkx6.1 in embryonic chicken spinal cord results in an induction of Olig2 expression at early stages, but an inhibition at later stages. Moreover, the regulation of Olig gene expression and oligodendrogenesis by Nkx6.1 also appears to be region specific. In the hindbrain, unlike in the spinal cord, Olig1and Olig2 can be expressed both inside and outside the Nkx6.1-expressing domains and oligodendrogenesis in this region is not dependent on Nkx6.1 activity.

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Region-specific and stage-dependent regulation of Olig gene expression and oligodendrogenesis byNkx6.1homeodomain transcription factor

Liu

Cai

et al. 2003

Development

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“…This recovery is probably because of the highly proliferative property of oligodendrocyte progenitors, as shown in the analysis of Pax6 mutant mice (Sun et al, 1998). The reduction of oligodendrocyte progenitors at E12.5 in the double mutants is likely attributable to decrease of neural progenitors because Notch signaling is impaired.…”

Section: Maintenance Of Neural Progenitors By Mash1 and Math3mentioning

confidence: 87%

Mash1andMath3Are Required for Development of Branchiomotor Neurons and Maintenance of Neural Progenitors

Ohsawa¹,

Ohtsuka²,

Kageyama³

2005

J. Neurosci.

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Basic helix-loop-helix (bHLH) transcription factors are known to play important roles in neuronal determination and differentiation. However, their exact roles in neural development still remain to be determined because of the functional redundancy. Here, we examined the roles of neural bHLH genes Mash1 and Math3 in the development of trigeminal and facial branchiomotor neurons, which derive from rhombomeres 2-4. In Math3-null mutant mice, facial branchiomotor neurons are misspecified, and both trigeminal and facial branchiomotor neurons adopt abnormal migratory pathways. In Mash1;Math3 double-mutant mice, trigeminal and facial branchiomotor neurons are severely reduced in number partly because of increased apoptosis. In addition, neurons with migratory defects are intermingled over the midline from either side of the neural tube. Furthermore, oligodendrocyte progenitors of rhombomere 4 are reduced in number. In the absence of Mash1 and Math3, expression of Notch signaling components is severely downregulated in rhombomere 4 and neural progenitors are not properly maintained, which may lead to intermingling of neurons and a decrease in oligodendrocyte progenitors. These results indicate that Mash1 and Math3 not only promote branchiomotor neuron development but also regulate the subsequent oligodendrocyte development and the cytoarchitecture by maintaining neural progenitors through Notch signaling.

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“…Oligodendrocyte precursors arise from a similar region of the neural tube that gives rise to motor neurons (Sun et al, 1998) and can be induced at an identical concentration of N-Shh in neural explant culture (Pringle et al, 1996). To determine whether oligodendrocyte precursors were induced in Shh-Tg mice, we performed immunolabeling with PDGF␣R (Pringle and Richardson, 1993).…”

Section: Induction Of Neuronal and Oligodendroglial Lineages In Hypermentioning

confidence: 99%

Sonic hedgehogRegulates Proliferation and Inhibits Differentiation of CNS Precursor Cells

et al. 1999

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Activation of the Sonic hedgehog (Shh) signal transduction pathway is essential for normal pattern formation and cellular differentiation in the developing CNS. However, it is also thought to be etiological in primitive neuroectodermal tumors. We adapted GAL4/UAS methodology to ectopically express full-length Shh in the dorsal neural tube of transgenic mouse embryos commencing at 10 d postcoitum (dpc), beyond the period of primary dorsal-ventral pattern formation and floorplate induction. Expression of Shh was maintained until birth, permitting us to investigate effects of ongoing exposure to Shh on CNS precursors in vivo. Proliferative rates of spinal cord precursors were twice that of wild-type littermates at 12.5 dpc. In contrast, at late fetal stages (18.5 dpc), cells that were Shh-responsive but postmitotic were present in persistent structures reminiscent of the ventricular zone germinal matrix. This tissue remained blocked in an undifferentiated state. These results indicate that cellular competence restricts the proliferative response to Shh in vivo and provide evidence that proliferation and differentiation can be regulated separately in precursor cells of the spinal cord. Thus, Hedgehog signaling may contribute to CNS tumorigenesis by directly enhancing proliferation and preventing neural differentiation in selected precursor cells.

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Pax6 Influences the Time and Site of Origin of Glial Precursors in the Ventral Neural Tube

Cited by 98 publications

References 49 publications

Region-specific and stage-dependent regulation of Olig gene expression and oligodendrogenesis byNkx6.1homeodomain transcription factor

Region-specific and stage-dependent regulation of Olig gene expression and oligodendrogenesis byNkx6.1homeodomain transcription factor

Mash1andMath3Are Required for Development of Branchiomotor Neurons and Maintenance of Neural Progenitors

Sonic hedgehogRegulates Proliferation and Inhibits Differentiation of CNS Precursor Cells

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