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Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (scRNA-seq - mus musculus)

ABSTRACT: We performed scRNA in sorted LinnegcKit+ bone marrow cells from single and double Bap1 and Trp53 knockout mice to identify transcirptional programs driving erythroleukemia.

ORGANISM(S): Mus musculus

PROVIDER: GSE266948 | GEO | 2026/03/18

REPOSITORIES: GEO

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Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (RNA-seq - mus musculus)

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Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (RNA-seq - mus musculus)

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Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (scRNA-seq - mus musculus)

Project description:Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (scRNA-seq - mus musculus)

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Expression data from BAP1 depleted cells

Project description:The deubiquitinase BAP1 is a candidate tumor suppressor regulating cell proliferation in human and is required for development in Drosophila. BAP1 is assembled into high molecular weight transcriptional multi-protein complexes. In order to identify potential BAP1 target genes, global mRNA expression profiling using microarrays was conducted. U2OS cells, transfected with a non-target control shRNA or shRNAs targeting BAP1, were selected with puromycin containing medium and then synchronized at the G1/S border to allow comparative analysis of gene expression.

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Genome wide binding sites of BAP1, HCF1 and OGT

Project description:We report the genome wide binding sites of BAP1, HCF1 and OGT in bone marrow derived macrophages. De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor–1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans. For BAP1, bone marrow derived macrophages were used differentiated from bone marrow cells of BAP1-3X Flag Tagged KI mice we generated. For OGT and HCF1, bone marrow derived macrophages were used from BAP1 WT mice.

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