Tlx, an Orphan Nuclear Receptor, Regulates Cell Numbers and Astrocyte Development in the Developing Retina

Miyawaki, T.; Dezawa, Mari; Yu, Ruth T.; Idé, Chizuka; Nishikawa, Shin‐Ichi; Honda, Yoshio; Tanabe, Yukito; Tanabe, Teruyo

doi:10.1523/jneurosci.2235-04.2004

Cited by 96 publications

(120 citation statements)

References 48 publications

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“…Tll is also expressed in undifferentiated proliferating neural precursor cells at the third instar larval stage, the last larval stage before eclosion into adult flies, indicating that tll may have an essential function in neuronal stem cells [11]. Consistent with the findings in Drosophila, mouse Tlx is expressed in the developing central nervous system (CNS) from embryonic day 8 (E8) until E13.5 and in retinal progenitor cells (RPCs) from E11.5 until E17.5 during retinal development [5,[30][31][32]. At the embryonic stage, Tlx expression presents a graded pattern in the telencephalon along the dorsalventral axis with a high level in the dorsal-lateral region and a low level in the ventral-medial region [33].…”

Section: Tlx Expression Its Targets and Related Signal Pathwaysmentioning

confidence: 63%

“…It controls the generation of proper numbers of RPCs by activating cyclin-D1 and p27 during early retinal layer formation [31]. Further, Tlx expression has been found in Müller glial cells and mature astrocytes of the inner nuclear layer after birth and temporarily in immature astrocytes before migration from the optic nerve to the inner nuclear layer [31]. Consistently, reduced retinal size and cell number, optic nerve degeneration, and visual impairment have been reported in Tlxdeficient mice [32,45,65].…”

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 85%

“…Drosophila tll drives embryonic cells into the fate of developing into optic lobes but not Bolwig's organ via antagonizing EGFR signaling [29]. Mouse Tlx is involved in eye development from early RPC differentiation to later astrocyte maturation [31]. It controls the generation of proper numbers of RPCs by activating cyclin-D1 and p27 during early retinal layer formation [31].…”

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 99%

“…Mouse Tlx is involved in eye development from early RPC differentiation to later astrocyte maturation [31]. It controls the generation of proper numbers of RPCs by activating cyclin-D1 and p27 during early retinal layer formation [31]. Further, Tlx expression has been found in Müller glial cells and mature astrocytes of the inner nuclear layer after birth and temporarily in immature astrocytes before migration from the optic nerve to the inner nuclear layer [31].…”

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 99%

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The Orphan Nuclear Receptor TLX/NR2E1 in Neural Stem Cells and Diseases

Wang

Xiong

2016

Neurosci. Bull.

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The human TLX gene encodes an orphan nuclear receptor predominantly expressed in the central nervous system. Tailess and Tlx, the TLX homologues in Drosophila and mouse, play essential roles in body-pattern formation and neurogenesis during early embryogenesis and perform crucial functions in maintaining stemness and controlling the differentiation of adult neural stem cells in the central nervous system, especially the visual system. Multiple target genes and signaling pathways are regulated by TLX and its homologues in specific tissues during various developmental stages. This review aims to summarize previous studies including many recent updates from different aspects concerning TLX and its homologues in Drosophila and mouse.

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Section: Tlx Expression Its Targets and Related Signal Pathwaysmentioning

confidence: 63%

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 85%

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 99%

Section: Roles Of Tlx Homologues In Regulation Of Retinal Progenitor mentioning

confidence: 99%

See 2 more Smart Citations

The Orphan Nuclear Receptor TLX/NR2E1 in Neural Stem Cells and Diseases

Wang

Xiong

2016

Neurosci. Bull.

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“…This interpretation is in keeping with the fact that N-cadherin is expressed in vascular endothelia (Luo and Radice, 2005;Navarro et al, 1998). The situation is less clear for M- (Tomi et al, 2004) and R-cadherin (Dorrell et al, 2002); the latter, however has been reported to be expressed in (retinal) astroglia (Miyawaki et al, 2004). This said, it follows from straightforward numerical considerations that most Math1-GFP negative cells expressing M-, N-and R-cadherin are indeed (postmitotic) granule cells.…”

Section: Comparison Of Our Cadherin Data With Previous Results -Qualimentioning

confidence: 84%

Expression of classical cadherins in the cerebellar anlage: Quantitative and functional aspects

Gliem

Weisheit

Mertz

et al. 2006

Molecular and Cellular Neuroscience

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During central nervous system (CNS) development, cell migration precedes and is key to the integration of diverse sets of cells. Mechanistically, CNS histogenesis is realized through a balanced interplay of cell-cell and cell-matrix adhesion molecules. Here, we summarize experiments that probe the developmental expression and potential significance of a set of cadherins, including M-, N and R-cadherin, for patterning of the cerebellar cortex. We established a transgenic marker that allows cerebellar granule cells to be followed from the neuroblast stage to their final, postmitotic settlement. In conjunction with flow-cytometry, this allowed us to derive a quantitative view of cadherin expression in differentiating granule cells and relate it to the expression of the same cadherins in cerebellar inhibitory interneuronal precursors. In vitro reaggregation analysis supports a role for cadherins in cell sorting and migration within the nascent cerebellar cortex that may be rationalized within the context of the differential adhesion hypothesis (Foty and Steinberg, 2005).

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Spatial patterning of cholinergic amacrine cells in the mouse retina

Whitney

Keeley

Raven

et al. 2008

J of Comparative Neurology

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The two populations of cholinergic amacrine cells in the inner nuclear layer (INL) and the ganglion cell layer (GCL) differ in their spatial organization in the mouse retina, but the basis for this difference is not understood. The present investigation examined this issue in six strains of mice that differ in their number of cholinergic cells, addressing how the regularity, packing, and spacing of these cells varies as a function of strain, layer, and density. The number of cholinergic cells was lower in the GCL than in the INL in all six strains. The nearest neighbor and Voronoi domain regularity indexes as well as the packing factor were each consistently lower for the GCL. While these regularity indexes and the packing factor were largely stable across variation in density, the effective radius was inversely related to density for both the GCL and INL, being smaller and more variable in the GCL. Consequently, despite the lower densities in the GCL, neighboring cells were more likely to be positioned closer to one another than in the higher-density INL, thereby reducing regularity and packing. This difference in the spatial organization of cholinergic cells may be due to the cells in the GCL having been passively displaced by fascicles of optic axons and an expanding retinal vasculature during development. In support of this interpretation, we show such displacement of cholinergic somata relative to their dendritic stalks and a decline in packing efficiency and regularity during postnatal development that is more severe for the GCL.

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Tlx, an Orphan Nuclear Receptor, Regulates Cell Numbers and Astrocyte Development in the Developing Retina

Cited by 96 publications

References 48 publications

The Orphan Nuclear Receptor TLX/NR2E1 in Neural Stem Cells and Diseases

The Orphan Nuclear Receptor TLX/NR2E1 in Neural Stem Cells and Diseases

Expression of classical cadherins in the cerebellar anlage: Quantitative and functional aspects

Spatial patterning of cholinergic amacrine cells in the mouse retina

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