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FBXO11-Mediated Proteolysis of BAHD1 Relieves PRC2-dependent Transcriptional Repression in Erythropoiesis

ABSTRACT: FBXO11-Mediated Proteolysis of BAHD1 Relieves PRC2-dependent Transcriptional Repression in Erythropoiesis

PROVIDER: PRJNA474683 | ENA |

REPOSITORIES: ENA

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FBXO11-Mediated Proteolysis of BAHD1 Relieves PRC2-dependent Transcriptional Repression in Erythropoiesis

Project description:The histone mark H3K27me3 and its reader/writer Polycomb repressive complex 2 (PRC2) mediate widespread transcriptional repression in stem and progenitor cells. Mechanisms that regulate this activity are critical for tissue development but poorly understood. Here we show that the E3 ubiquitin ligase FBXO11 relieves PRC2-mediated repression during erythroid maturation by targeting its newly identified substrate BAHD1, an H3K27me3 reader that recruits transcriptional co-repressors. Erythroblasts lacking FBXO11 are developmentally delayed, with reduced expression of maturation-associated genes, most of which harbor bivalent histone marks (activating H3K4me3 and repressive H3K27me3), bind BAHD1, and fail to recruit the erythroid transcription factor GATA1. The BAHD1 complex interacts physically with PRC2 and depletion of either component restores FBXO11-deficient erythroid gene expression. Previous studies showed that FBXO11 promotes B-cell development and inhibits lymphomagenesis by degrading the transcriptional repressor BCL6. We show that in aggressive B-cell lymphoma lines, depletion of FBXO11 causes the accumulation of both BCL6 and BAHD1, and that suppression of BAHD1 slows cell expansion. Our studies identify BAHD1 as a novel effector of PRC2-mediated repression and reveal how a single E3 ubiquitin ligase eliminates PRC2 repression at developmentally poised bivalent genes during erythropoiesis. The FBXO11-BAHD1 regulatory axis may function in other developmental pathways, including B-lymphopoiesis and lymphomagenesis.

2020-12-31 | GSE115357 | GEO

FBXO11-mediated proteolysis of BAHD1 relieves PRC2-dependent transcriptional repression in erythropoiesis.

Project description: Not available

| S-EPMC7820877 | biostudies-literature

BAHD1

Project description:BAHD1

| PRJNA672984 | ENA

Chromatin immunoprecipitation-sequencing of HEK293 cells (HEK293-HPT-blue) and HEK293 cells stably over-expressing the BAHD1 gene (HEK293-HPT-BAHD1)

Project description:We report the genomic occupancy of the BAHD1 protein in HEK293 cells over-expressing the BAHD1 gene (HEK293-HPT-BAHD1)

2015-12-11 | GSE53372 | GEO

Transcriptome of HEK293 cells (HEK293-CT) and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

Project description:Comparison of gene expression profile of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

2015-12-11 | GSE51863 | GEO

Transcriptome of BAHD1 knock-down HEK293 cells with siRNA

Project description:Gene silencing via heterochromatin formation plays a major role in cell differentiation and maintenance of homeostasis. Here, we report the identification and characterization of a novel heterochromatinization factor in vertebrates, Bromo Adjacent Homology Domain-containing protein 1 (BAHD1). BAHD1 interacts with HP1, MBD1, HDAC5 and with several transcription factors. Through electron and immunofluorescence microscopy studies, we show that BAHD1 overexpression directs HP1 to specific nuclear sites and promotes formation of large heterochromatic domains, which lack acetyl histone H3 and are enriched in H3 trimethylated at lysine 27. Furthermore, ectopically expressed BAHD1 colocalizes with the heterochromatic X inactive chromosome. As highlighted by whole genome microarray analysis of BAHD1 knock down cells, BAHD1 represses several proliferation and survival genes and in particular, the insulin-like growth factor II gene (IGF2). BAHD1 specifically binds the CpG-rich P3 promoter of IGF2. This region contains DNA binding sequences for the transcription factor SP1, with which BAHD1 co-immunoprecipitates. Collectively, these findings provide evidence that BAHD1 acts as a silencer by recruiting proteins that coordinate heterochromatin assembly at specific sites in the genome. We used microarrays to identify BAHD1 gene targets. We compared the transcriptome profile of BAHD1 depleted cells with siRNA to that of cells treated with control siRNA.

2009-07-16 | GSE16097 | GEO

Methylated DNA immunoprecipitation-sequencing of HEK293 cells (HEK293-CT) and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

Project description:we report the partial methylome (CG-rich regions) of HEK293 cells and HEK293 cells over-expressing the BAHD1 gene (HEK-BAHD1)

2015-12-11 | GSE51864 | GEO

Transcriptome of HEK293 cells (HEK293-CT) and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

Project description:Comparison of gene expression profile of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1) We used micrarrays to identify the repertoire of genes differentially expressed upon overexpression of the chromatin repressor BAHD1 in HEK293 cells.

2015-12-11 | E-GEOD-51863 | biostudies-arrayexpress

whole-genome bisulfite sequencing (BS-seq) of HEK293 cells (HEK293-CT) and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

Project description:Comparison of methylome of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)

2015-12-11 | GSE51867 | GEO

Mtf2-PRC2 control of canonical Wnt signaling is required for definitive erythropoiesis [RNA-Seq]

Project description:Polycomb repressive complex 2 (PRC2) accessory proteins play substoichiometric, tissue-specific roles to recruit PRC2 to specific genomic loci or increase enzymatic activity, while PRC2 core proteins are required for complex stability and global levels of trimethylation of histone 3 at lysine 27 (H3K27me3). Here, we demonstrate a role for the classical PRC2 accessory protein Mtf2/Pcl2 in the hematopoietic system that is more akin to that of a core PRC2 protein. Mtf2-/- erythroid progenitors demonstrate markedly decreased core PRC2 protein levels and a global loss of H3K27me3 at promoter-proximal regions. The resulting de-repression of transcriptional and signaling networks blocks definitive erythroid development, culminating in Mtf2-/- embryos dying by e15.5 due to severe anemia. Gene regulatory network (GRN) analysis demonstrated Mtf2 directly regulates Wnt signaling in erythroblasts, leading to activated canonical Wnt signaling in Mtf2-deficient erythroblasts, while chemical inhibition of canonical Wnt signaling rescued Mtf2-deficient erythroblast differentiation in vitro. Using a combination of in vitro, in vivo and systems analyses, we demonstrate that Mtf2 is a critical epigenetic regulator of Wnt signaling during erythropoiesis and recast the role of polycomb accessory proteins in a tissue-specific context.

2018-07-26 | GSE72286 | GEO

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