Genetic Patterning of the mammalian telencephalon by morphogenetic molecules and transcription factors

Takahashi, Hiroshi; Liu, Fu-Chin

doi:10.1002/bdrc.20077

Cited by 43 publications

(28 citation statements)

References 128 publications

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“…Cerebral cortex arealizationor patterning is controlled by the expression of a great repertoire of transcription factors that define neural stem cells and progenitors generation, self-renewal and phenotypes. Those factors, such as FoxG1, are modulated by diverse morphogenetic proteins distinctly distributed in different patterning centers (Takahashi and Liu, 2006; O’Leary and Sahara, 2008). …”

Section: Resultsmentioning

confidence: 99%

TGF-Î²1 promotes cerebral cortex radial glia-astrocyte differentiation in vivo

Stipursky

Francis

Dezonne

et al. 2014

Front. Cell. Neurosci.

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The major neural stem cell population in the developing cerebral cortex is composed of the radial glial cells, which generate glial cells and neurons. The mechanisms that modulate the maintenance of the radial glia (RG) stem cell phenotype, or its differentiation, are not yet completely understood. We previously demonstrated that the transforming growth factor-β1 (TGF-β1) promotes RG differentiation into astrocytes in vitro (Glia 2007; 55:1023-33) through activation of multiple canonical and non-canonical signaling pathways (Dev Neurosci 2012; 34:68-81). However, it remains unknown if TGF-β1 acts in RG-astrocyte differentiation in vivo. Here, we addressed the astrogliogenesis induced by TGF-β1 by using the intraventricular in utero injection in vivo approach. We show that injection of TGF-β1 in the lateral ventricles of E14,5 mice embryos resulted in RG fibers disorganization and premature gliogenesis, evidenced by appearance of GFAP positive cells in the cortical wall. These events were followed by decreased numbers of neurons in the cortical plate (CP). Together, we also described that TGF-β1 actions are region-dependent, once RG cells from dorsal region of the cerebral cortex demonstrated to be more responsive to this cytokine compared with RG from lateral cortex either in vitro as well as in vivo. Our work demonstrated that TGF-β1 is a critical cytokine that regulates RG fate decision and differentiation into astrocytes in vitro and in vivo. We also suggest that RG cells are heterogeneous population that acts as distinct targets of TGF-β1 during cerebral cortex development.

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Section: Resultsmentioning

confidence: 99%

TGF-Î²1 promotes cerebral cortex radial glia-astrocyte differentiation in vivo

Stipursky

Francis

Dezonne

et al. 2014

Front. Cell. Neurosci.

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“…The brain regulates facial development The regulatory mechanisms controlling Shh expression in the neural tube are complex and involve multiple enhancers (Epstein et al, 2000;Epstein et al, 1999;Jeong et al, 2006;Jeong and Epstein, 2003) and signals (reviewed by Takahashi and Liu, 2006). However, published data indicate that a cis-regulatory element controlling Shh expression in the telencephalon contains an Nkx2.1-binding site (Jeong et al, 2006), and Shh expression is absent from the telencephalon in the Nkx2.1 -/-mouse (Sussel et al, 1999).…”

Section: Research Articlementioning

confidence: 99%

A SHH-responsive signaling center in the forebrain regulates craniofacial morphogenesis via the facial ectoderm

2009

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Interactions among the forebrain, neural crest and facial ectoderm regulate development of the upper jaw. To examine these interactions, we activated the Sonic hedgehog (SHH) pathway in the brain. Beginning 72 hours after activation of the SHH pathway, growth within the avian frontonasal process (FNP) was exaggerated in lateral regions and impaired in medial regions. This growth pattern is similar to that in mice and superimposed a mammalian-like morphology on the upper jaw. Jaw growth is controlled by signals from the frontonasal ectodermal zone (FEZ), and the divergent morphologies that characterize birds and mammals are accompanied by changes in the FEZ. In chicks there is a single FEZ spanning the FNP, but in mice both median nasal processes have a FEZ. In treated chicks, the FEZ was split into right and left domains that resembled the pattern present in mice. Additionally, we observed that, in the brain, fibroblast growth factor 8 (Fgf8) was downregulated, and signals in or near the nasal pit were altered. Raldh2 expression was expanded, whereas Fgf8, Wnt4, Wnt6 and Zfhx1b were downregulated. However, Wnt9b, and activation of the canonical WNT pathway, were unaltered in treated embryos. At later time points the upper beak was shortened owing to hypoplasia of the skeleton, and this phenotype was reproduced when we blocked the FGF pathway. Thus, the brain establishes multiple signaling centers within the developing upper jaw. Changes in organization of the brain that occur during evolution or as a result of disease can alter these centers and thereby generate morphological variation.

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“…As a result, the location of a cell along the apical-basal axis provides information on its proliferation status (Dehay and Kennedy, 2007;Götz and Huttner, 2005;Takahashi and Liu, 2006). To determine whether Mcl1 affects the proliferation status of NPCs, Ctl, Mcl1 or mt Mcl1 plasmids were electroporated into E13 embryos.…”

Section: Mcl1 Protein Is Tightly Regulated In Npcsmentioning

confidence: 99%

Mcl1 regulates the terminal mitosis of neural precursor cells in the mammalian brain through p27Kip1

et al. 2013

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SUMMARYCortical development requires the precise timing of neural precursor cell (NPC) terminal mitosis. Although cell cycle proteins regulate terminal mitosis, the factors that influence the cell cycle machinery are incompletely understood. Here we show in mice that myeloid cell leukemia 1 (Mcl1), an anti-apoptotic Bcl-2 protein required for the survival of NPCs, also regulates their terminal differentiation through the cell cycle regulator p27 Kip1 . A BrdU-Ki67 cell profiling assay revealed that in utero electroporation of Mcl1 into NPCs in the embryonic neocortex increased NPC cell cycle exit (the leaving fraction

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Genetic Patterning of the mammalian telencephalon by morphogenetic molecules and transcription factors

Cited by 43 publications

References 128 publications

TGF-Î²1 promotes cerebral cortex radial glia-astrocyte differentiation in vivo

TGF-Î²1 promotes cerebral cortex radial glia-astrocyte differentiation in vivo

A SHH-responsive signaling center in the forebrain regulates craniofacial morphogenesis via the facial ectoderm

Mcl1 regulates the terminal mitosis of neural precursor cells in the mammalian brain through p27Kip1

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