Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells

Masahira, Noritaka; Takebayashi, Hirohide; Ono, Katsuhiko; Watanabe, Keisuke; Ding, Lei; Furusho, Miki; Ogawa, Yasuhiro; Nabeshima, Yo‐ichi; Alvarez-Buylla, Arturo; Shimizu, Katsuji; Ikenaka, Kazuhiro

doi:10.1016/j.ydbio.2006.02.029

Cited by 169 publications

(151 citation statements)

References 54 publications

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“…This is in pronounced contrast to the multitude of lineages observed to arise from this progenitor pool during development using even the very same mouse line Masahira et al, 2006;Miyoshi et al, 2007;Ono et al, 2008) or the NG2::CreERTM T2 line (Zhu et al, 2008). Importantly, during development, the different cell types arise from distinct sets of Olig2 ϩ progenitors (e.g., Olig2 ϩ cells that generate motoneurons do not share their lineage with those that generate oligodendrocytes) (Mukouyama et al, 2006;Wu et al, 2006).…”

Section: Progeny Of Olig2-expressing Cells In the Adult Versus Develomentioning

confidence: 83%

“…The transcription factor Olig2 is a necessary regulator of oligodendrocyte and motoneurons development, and Olig2-expressing cells also generate cholinergic neurons, ependymal cells, as well as some astrocytes during development (Takebayashi et al, 2002;Ligon et al, 2006a;Masahira et al, 2006;Cai et al, 2007;Ono et al, 2008). Interestingly, Olig2 is also required for the specification of NG2 ϩ cells (Ligon et al, 2006b).…”

Section: Introductionmentioning

confidence: 99%

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Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Dimou¹,

Simon²,

Kirchhoff³

et al. 2008

J. Neurosci.

478

564

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Despite their abundance, still little is known about the rather frequent, constantly proliferating progenitors spread throughout the adult mouse brain parenchyma. The majority of these progenitors express the basic-helix-loop-helix transcription factor Olig2, and their number further increases after injury. Here, we examine the progeny of this progenitor population by genetic fate mapping using tamoxifen-inducible Cre-recombination in the Olig2 locus to turn on permanent reporter gene expression in the adult brain. Consistent with Olig2 expression in proliferating NG2 ϩ progenitors, most reporter ϩ cells seen shortly after initiating recombination at adult stages incorporated BrdU and contained the proteoglycan NG2 in both the gray (GM) and the white matter (WM) of the cerebral cortex. However, at longer time points after induction, we observed profound differences in the identity of reporter ϩ cells in the WM and GM. Whereas most of the Olig2 ϩ progenitors had generated mature, myelinating oligodendrocytes in the WM, hardly any reporter ϩ cells showing mature oligodendrocyte characteristics were detectable even up to 6 months after recombination in the GM. In the GM, most reporter ϩ cells remained NG2 ϩ , even after injury, but stopped proliferating rather soon after recombination. Thus, our results demonstrate the continuous generation of mature, myelinating oligodendrocytes in the WM, whereas cells in the GM generated mostly postmitotic NG2 ϩ glia.

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Section: Progeny Of Olig2-expressing Cells In the Adult Versus Develomentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Dimou¹,

Simon²,

Kirchhoff³

et al. 2008

J. Neurosci.

478

564

View full text Add to dashboard Cite

show abstract

“…Using immunoreactivity to localize phosphorylated ERK1/2 in the developing chick spinal cord and dorsal root ganglia, Kato et al showed that pERK1/2 is co-localized to Olig2 positive cells in embryonic day 7 chick spinal cords. Olig2 encodes a transcription factor that is essential for motor neuron and OL development [44,45]. Due to other circumstantial evidence relating to the location of the pERK1/2, Kato et al [43] concluded that pERK1/2 plays a role in the regulation of OP migration.…”

Section: Erk Regulates Pdgf Induction Of Op Migrationmentioning

confidence: 99%

Initiation of Oligodendrocyte Progenitor Cell Migration by a PDGF-A Activated Extracellular Regulated Kinase (ERK) Signaling Pathway

et al. 2008

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During CNS development, oligodendrocyte progenitor (OP) cells migrate from germinal zones to presumptive white matter tracts to generate myelinating oligodendrocytes. In vitro and in vivo studies indicate that platelet-derived growth factor-A (PDGF-A) is a potent chemoattractant for OP cells and important for normal distribution throughout the developing CNS. However, PDGF-A does not localize in concentration gradients corresponding to OP migratory pathways, as would be expected for a chemoattractant to direct migration. Therefore, the mechanism by which PDGF-A regulates OP distribution remains to be clarified. Here we show that PDGF-A induces OP migration and continuous exposure to PDGF-A is not required to maintain migration. Using pharmacological inhibitors, we show that a self-sustaining extracellular-regulated-kinase signaling pathway drives OP migration for up to 72 hours after the initial PDGF stimulus. These findings indicate PDGF-A may act to mobilize OP cells that then respond to distinct directional signals to distribute appropriately within the CNS.

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“…Several transcription factors have been identified that are necessary for OPC and OL generation. These include SOX10, OLIG1, and OLIG2, and homeodomain proteins of the Nkx family (Wegner, 2001;Stolt et al, 2002;Zhou and Anderson, 2002;Masahira et al, 2006;Nakamura et al, 2006;Wu et al, 2006). These various transcription factors are expressed by both OPCs and OLs, and mutations in some of these genes lead to the loss of OPCs as well as OLs.…”

Section: Introductionmentioning

confidence: 99%

Functional Genomic Analysis of Oligodendrocyte Differentiation

Dugas¹,

Tai²,

Speed³

et al. 2006

J. Neurosci.

294

353

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To better understand the molecular mechanisms governing oligodendrocyte (OL) differentiation, we have used gene profiling to quantitatively analyze gene expression in synchronously differentiating OLs generated from pure oligodendrocyte precursor cells in vitro. By comparing gene expression in these OLs to OLs generated in vivo, we discovered that the program of OL differentiation can progress normally in the absence of heterologous cell-cell interactions. In addition, we found that OL differentiation was unexpectedly prolonged and occurred in at least two sequential stages, each characterized by changes in distinct complements of transcription factors and myelin proteins. By disrupting the normal dynamic expression patterns of transcription factors regulated during OL differentiation, we demonstrated that these sequential stages of gene expression can be independently controlled. We also uncovered several genes previously uncharacterized in OLs that encode transmembrane, secreted, and cytoskeletal proteins that are as highly upregulated as myelin genes during OL differentiation. Last, by comparing genomic loci associated with inherited increased risk of multiple sclerosis (MS) to genes regulated during OL differentiation, we identified several new positional candidate genes that may contribute to MS susceptibility. These findings reveal a previously unexpected complexity to OL differentiation and suggest that an intrinsic program governs successive phases of OL differentiation as these cells extend and align their processes, ensheathe, and ultimately myelinate axons.

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Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells

Cited by 169 publications

References 54 publications

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Initiation of Oligodendrocyte Progenitor Cell Migration by a PDGF-A Activated Extracellular Regulated Kinase (ERK) Signaling Pathway

Functional Genomic Analysis of Oligodendrocyte Differentiation

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