Sagittal band expression of COUP-TF2 gene in the developing cerebellum

Yamamoto, Miyuki; Fujinuma, Masahiro; Tanaka, Manami; Dräger, Ursula C.; McCaffery, Peter

doi:10.1016/s0925-4773(99)00054-4

Cited by 6 publications

(7 citation statements)

References 7 publications

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“…Interestingly, COUP-TF is expressed in immature Purkinje cells and diminishes in expression as the Pcp-2 gene becomes TH-responsive (86). It is likely that the COUP-TF isoform detected in these studies is COUP-TFII as expression of this gene is maximal in the late gestation cerebellum and significantly reduced by PN7.5 (97). Additionally, recently published data reveal a Purkinje cell specific expression pattern for COUP-TFII but not COUP-TFI (96).…”

Section: Th Deiodination and The Developing Cerebellummentioning

confidence: 66%

“…Additionally, COUP-TFs repress gene expression by interacting with nuclear receptor corepressors (95). COUP-TFI and II are highly expressed in the developing brain (94,96,97) and are critically important for normal neural development as COUP-TFI null mice exhibit significant neuropathology (98). COUP-TFI specifically represses TH-dependent activation of the Pcp-2 promoter (86).…”

Section: Th Deiodination and The Developing Cerebellummentioning

confidence: 99%

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Thyroid hormone and cerebellar development

Anderson

2008

Cerebellum

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Thyroid hormone (TH) plays a key role in mammalian brain development. The developing brain is sensitive to both TH deficiency and excess. Brain development in the absence of TH results in motor skill deficiencies and reduced intellectual development. These functional abnormalities can be attributed to maldevelopment of specific cell types and regions of the brain including the cerebellum. TH functions at the molecular level by regulating gene transcription. Therefore, understanding how TH regulates cerebellar development requires identification of TH-regulated gene targets and the cells expressing these genes. Additionally, the process of TH-dependent regulation of gene expression is tightly controlled by mechanisms including regulation of TH transport, TH metabolism, toxicologic inhibition of TH signaling, and control of the nuclear TH response apparatus. This review will describe the functional, cellular, and molecular effects of TH deficit in the developing cerebellum and emphasize the most recent findings regarding TH action in this important brain region.

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Section: Th Deiodination and The Developing Cerebellummentioning

confidence: 66%

Section: Th Deiodination and The Developing Cerebellummentioning

confidence: 99%

Thyroid hormone and cerebellar development

Anderson

2008

Cerebellum

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“…The first one cloned was designed as COUP-TFI (Wang et al, 1989) or v-ErbA-related protein 3, EAR-3 (Miyajima et al, 1988), while the second member was named COUP-TFII (Ritchie et al, 1990; Wang et al, 1991) or apolipoprotein regulating protein 1, ARP1 (Ladias and Karathanasis, 1991). Previous in situ hybridization data showed that COUP-TFII is expressed in the ventral part of the thalamus, hypothalamus, midbrain, and cerebellum (Qiu et al, 1994; Yamamoto et al, 1999). Interestingly, the expression of COUP-TFII is restricted in sagittal bands in the cerebellum at early embryonic days (Yamamoto et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) regulates growth and patterning of the postnatal mouse cerebellum

Kim

Takamoto

Yan

et al. 2009

Developmental Biology

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COUP-TFII (also known as Nr2f2), a member of the nuclear orphan receptor superfamily, is expressed in several regions of the central nervous system (CNS), including the ventral thalamus, hypothalamus, midbrain, pons, and spinal cord. To address the function of COUP-TFII in the CNS, we generated conditional COUP-TFII knockout mice using a tissue-specific NSE-Cre recombinase. Ablation of COUP-TFII in the brain resulted in malformation of the lobule VI in the cerebellum and a decrease in differentiation of cerebellar neurons and cerebellar growth. The decrease in cerebellar growth in NSECre/+/CIIF/F mice is due to reduced proliferation and increased apoptosis in granule cell precursors (GCPs). Additional studies demonstrated that insulin like growth factor 1 (IGF-1) expression was reduced in the cerebellum of NSECre/+/CIIF/F mice, thereby leading to decreased Akt1 and GSK-3β activities, and the reduced expression of mTOR. Using ChIP assays, we demonstrated that COUP-TFII was recruited to the promoter region of IGF-1 in a Sp1-dependent manner. In addition, dendritic branching of Purkinje cells was decreased in the mutant mice. Thus, our results indicate that COUP-TFII regulates growth and maturation of the mouse postnatal cerebellum through modulation of IGF-1 expression.

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“…To determine if RERE was expressed in Purkinje cells at various times during cerebellar development, we used two different Purkinje cells markers: NR2F2, which is also known to be expressed in Purkinje cells during the early stages of cerebellar development [26], [27], [44] and calbindin which is a well-known marker for post-mitotic Purkinje cells [28]. At E18.5, a subset of Purkinje cells was positive for both RERE and NR2F2 antibodies but expression of RERE was not detected in all NR2F2-expressing cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…To do so, we used NR2F2 as a marker for early Purkinje cells since it is known to be expressed in the cerebellar analge as early as E13.0 and in migrating Purkinje cells starting at E15.5 [27]. In the cerebellums of wild-type embryos at E18.5, most NR2F2-positive cells were located in the PCL and only a few NR2F2-positive cells were identified in the center of cerebellar cortex (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mouse Model Reveals the Role of RERE in Cerebellar Foliation and the Migration and Maturation of Purkinje Cells

Kim

Scott

2014

PLoS ONE

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Nuclear receptors and their coregulators play a critical role in brain development by regulating the spatiotemporal expression of their target genes. The arginine-glutamic acid dipeptide repeats gene (Rere) encodes a nuclear receptor coregulator previously known as Atrophin 2. In the developing cerebellum, RERE is expressed in the molecular layer, the Purkinje cell layer and the granule cell layer but not in granule cell precursors. To study RERE's role in cerebellar development, we used RERE-deficient embryos bearing a null allele (om) and a hypomorphic allele (eyes3) of Rere (Rere om/eyes3). In contrast to wild-type embryos, formation of the principal fissures in these RERE-deficient embryos was delayed and the proliferative activity of granule cell precursors (GCPs) was reduced at E18.5. This reduction in proliferation was accompanied by a decrease in the expression of sonic hedgehog (SHH), which is secreted from Purkinje cells and is required for normal GCP proliferation. The maturation and migration of Purkinje cells in Rere om/eyes3 embryos was also delayed with decreased numbers of post-migratory Purkinje cells in the cerebellum. During the postnatal period, RERE depletion caused incomplete division of lobules I/II and III due to truncated development of the precentral fissure in the cerebellar vermis, abnormal development of lobule crus I and lobule crus II in the cerebellar hemispheres due to attenuation of the intercrural fissure, and decreased levels of Purkinje cell dendritic branching. We conclude that RERE-deficiency leads to delayed development of the principal fissures and delayed maturation and migration of Purkinje cells during prenatal cerebellar development and abnormal cerebellar foliation and Purkinje cell maturation during postnatal cerebellar development.

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Sagittal band expression of COUP-TF2 gene in the developing cerebellum

Cited by 6 publications

References 7 publications

Thyroid hormone and cerebellar development

Thyroid hormone and cerebellar development

Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) regulates growth and patterning of the postnatal mouse cerebellum

Mouse Model Reveals the Role of RERE in Cerebellar Foliation and the Migration and Maturation of Purkinje Cells

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