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Expression data from Mouse embryo

ABSTRACT: Mice lacking the function of the PcG protein CBX2 (also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes. To clarify the molecular basis of the defects, RNA prepared from both wild type and KO gonads were subjected to microarray analyses.

ORGANISM(S): Mus musculus

PROVIDER: GSE29485 | GEO | 2011/07/01

SECONDARY ACCESSION(S): PRJNA141643

REPOSITORIES: GEO

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Expression data from Mouse embryo

Project description:Mice lacking the function of the PcG protein CBX2 (also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes. To clarify the molecular basis of the defects, RNA prepared from both wild type and KO gonads were subjected to microarray analyses. Mouse embryonic gonads of Cbx2 knockout (KO) were sectioned and recovered at E11.5 for RNA extraction and hybridization on Affymetrix microarrays. Four different genotypes of embryos at E11.5 (XY WT, XX WT, XY Cbx2 KO, and XX Cbx2 KO) were frozen in OCT compound without fixation. They were sectioned to 30 μm slices and stained with hematoxylin. The developing gonadal cells localized by GATA4 immunostaining and morphology were prepared using a Laser Microdissection System. The specimens prepared from two or three individuals were combined into one group, and three groups were prepared for each genotype.

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2011-11-01 | GSE21650 | GEO

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The HDAC inhibitor SAHA regulates CBX2 stability via a SUMO-triggered ubiquitin-mediated pathway in leukemia

Project description:Leukemias are characterized by bone marrow failure due to oncogenic mutations of hematopoietic stem cells (HSC) or blood precursor cells. HSC differentiation and self-renewal properties are tightly regulated by Polycomb group (PcG) proteins, a well-characterized family of transcriptional epigenetic regulators. PcG proteins form two canonical complexes: Polycomb repressive complex 1 (PRC1), and Polycomb repressive complex 2 (PRC2).CBX proteins link the activity of PRC1 with PRC2, serving as critical regulators of PcG-mediating activity. While the functional role of some CBX proteins in cancer has been largely explored, recent reports support the specific role of CBX2 in human tumors, thus it represent a promising new target for anti-cancer strategies. To date, chromodomain inhibitors have been identified for CBX7 , but no molecules inhibiting CBX2 have been described. Nevertheless, different chromatin-modulating drugs such as histone deacetylase inhibitors (HDACi) are reported to regulate CBX2 targets on chromatin, suggesting that HDACi might be used to indirectly modulate aberrant effects of CBX2 in cancer. We describe a novel SAHA-mediated mechanism of CBX2 post-translational regulation. We found that CBX2 undergoes SAHA-induced SUMO2/3 modification and that CBX2 SUMOylation promotes its ubiquitination and proteasome-dependent degradation. We also identified the specific molecular pathway and key players regulating CBX2 stability, demonstrating that CBX4 and RNF4 act as the E3 SUMO and E3 ubiquitin ligase, respectively. Additionally, CBX2-depleted leukemic cells display impaired proliferation, showing that CBX2 is required for leukemia cell clonogenicity. Our study provides the first evidence of a non-canonical SAHA-mediated anti-tumorigenic activity via CBX2 SUMOylation and degradation

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