Identification of a novel transcriptional corepressor, Corl2, as a cerebellar Purkinje cell-selective marker

Minaki, Yasuko; Nakatani, Tomoya; Mizuhara, Eri; Inoue, Takeshi; Ono, Yūichi

doi:10.1016/j.gep.2008.04.004

Cited by 71 publications

(68 citation statements)

References 16 publications

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“…2S-V). Corl2 (Skor2 -Mouse Genome Informatics) expression, which labels PNs as they become postmitotic (Minaki et al, 2008), is also slightly reduced in the E14.5 and E16.5 Rp58 mutant (Fig. 2AA-HH).…”

Section: E-h) Pax6mentioning

confidence: 99%

“…ISH was performed as previously described (Tiveron et al, 1996). DIGlabeled antisense riboprobes were generated from linearized plasmids: Ascl1 (Lo et al, 1991), Atoh1 (Helms and Johnson, 1998), Corl2 (Minaki et al, 2008), cyclin D2 (Ciemerych et al, 2002), Neurod1 (Allen Brain Atlas, http://mouse.brain-map.org/experiment/show/75650865), Ngn1 (Ma et al, 1996), Ngn2 (Gradwohl et al, 1996), Pax2 (Nornes et al, 1990), Ptf1a (Pascual et al, 2007), Rp58 (Tatard et al, 2010) and Zic1 (Aruga et al, 1996).…”

Section: Immunohistochemistry and In Situ Hybridization (Ish)mentioning

confidence: 99%

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Rp58 is essential for the growth and patterning of the cerebellum and for glutamatergic and GABAergic neuron development

et al. 2012

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SUMMARYCerebellum development depends on the correct differentiation of progenitors into neurons, a process controlled by a transcriptional program that remains poorly understood. Here we show that neural-specific deletion of the BTB/POZ zinc-finger transcription factor-encoding gene Rp58 (Znf238, Zfp238) causes severe cerebellar hypoplasia and developmental failure of Purkinje neurons, Bergmann glia and granule neurons. Deletion of Rp58 in mouse embryonic Atoh1 + progenitors leads to strong defects in growth and foliation owing to its crucial role in the differentiation of granule neurons. Analysis of the Rp58 mutant at E14.5 demonstrates that Rp58 is required for the development of both glutamatergic and GABAergic neurons. Rp58 mutants show decreased proliferation of glutamatergic progenitors at E14.5. In addition, Rp58 ablation results in a reduced number of GABAergic Pax2 + neurons at E16.5 together with defects in the transcriptional program of ventricular zone progenitors. Our results indicate that Rp58 is essential for the growth and organization of the cerebellum and regulates the development of both GABAergic and glutamatergic neurons.

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Section: E-h) Pax6mentioning

confidence: 99%

Section: Immunohistochemistry and In Situ Hybridization (Ish)mentioning

confidence: 99%

Rp58 is essential for the growth and patterning of the cerebellum and for glutamatergic and GABAergic neuron development

et al. 2012

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“…Transcription factor Pax2 is involved in both cerebellar primordium specification and interneuron commitment, albeit at different developmental stages (Bouchard et al, 2000;Maricich and Herrup, 1999;Weisheit et al, 2006). Transcription factor orphan nuclear receptor Rorα, and c-Ski family member and transcription regulator Corl2 (also known as Skor2), are both expressed in the Purkinje cells and are necessary for their differentiation and maturation (Gold et al, 2003;Hamilton et al, 1996;Minaki et al, 2008;Nakagawa et al, 1997;Nakatani et al, 2014). Mutations of these signaling molecules and transcription factors often lead to congenital cerebellar conditions including cerebellar agenesis and hypoplasia that is associated with DandyWalker syndrome (Gold et al, 2003;Hamilton et al, 1996;Millen et al, 2014;Nakagawa et al, 1997;Parisi and Dobyns, 2003).…”

Section: Introductionmentioning

confidence: 99%

Polycomb Ezh2 controls the fate of GABAergic neurons in the embryonic cerebellum

et al. 2016

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Although the genetic interactions between signaling pathways and transcription factors have been largely decoded, much remains to be learned about the epigenetic regulation of cerebellar development. Here, we report that cerebellar deletion of Ezh2, the methyltransferase subunit of the PRC2 complex, results in reduced H3K27me3 and profound transcriptional dysregulation, including that of a set of transcription factors directly involved in cerebellar neuronal cell-type specification and differentiation. Such transcriptional changes lead to increased GABAergic interneurons and decreased Purkinje cells. Transcriptional changes also inhibit the proliferation of granule precursor cells derived from the rhombic lip. The loss of both cell types ultimately results in cerebellar hypoplasia. These findings indicate Ezh2/PRC2 plays crucial roles in regulating neurogenesis from both cerebellar germinal zones.

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“…In cell culture, mouse Corl1 functioned as a co-factor for the LBX1 homeodomain protein (Mizuhara et al, 2005). Mouse Corl2 was subsequently cloned and found to have neural-specific expression similar to mouse Corl1 -starting at embryonic day 10.5 in the cell bodies of Purkinje cell progenitors and in the Purkinje cells of adults (Minaki et al, 2008;Miyata et al, 2010). Interestingly, the cerebellum is the site of motor coordination and cerebellar defects are associated with movement disorders known as ataxias (Orr, 2010).…”

Section: Introductionmentioning

confidence: 99%

DrosophilaCORL is required for Smad2-mediated activation of Ecdysone Receptor expression in the mushroom body

et al. 2012

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SUMMARYCORL proteins (FUSSEL/SKOR proteins in humans) are related to Sno/Ski oncogenes but their developmental roles are unknown. We have cloned Drosophila CORL and show that its expression is restricted to distinct subsets of cells in the central nervous system. We generated a deletion of CORL and noted that homozygous individuals rarely survive to adulthood. Df(4)dCORL adult escapers display mushroom body (MB) defects and Df(4)dCORL larvae are lacking Ecdysone Receptor (EcR-B1) expression in MB neurons. This is phenocopied in CORL-RNAi and Smad2-RNAi clones in wild-type larvae. Furthermore, constitutively active Baboon (type I receptor upstream of Smad2) cannot stimulate EcR-B1 MB expression in Df(4)dCORL larvae, which demonstrates a formal requirement for CORL in Smad2 signaling. Studies of mouse Corl1 (Skor1) revealed that it binds specifically to Smad3. Overall, the data suggest that CORL facilitates Smad2 activity upstream of EcR-B1 in the MB. The conservation of neural expression and strong sequence homology of all CORL proteins suggests that this is a new family of Smad co-factors.

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Identification of a novel transcriptional corepressor, Corl2, as a cerebellar Purkinje cell-selective marker

Cited by 71 publications

References 16 publications

Rp58 is essential for the growth and patterning of the cerebellum and for glutamatergic and GABAergic neuron development

Rp58 is essential for the growth and patterning of the cerebellum and for glutamatergic and GABAergic neuron development

Polycomb Ezh2 controls the fate of GABAergic neurons in the embryonic cerebellum

DrosophilaCORL is required for Smad2-mediated activation of Ecdysone Receptor expression in the mushroom body

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