The Polycomb Group protein Rnf2/Ring1b is essential for zebrafish development and cardiogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA459724 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7119790_1.fastq.gz | Fastqsanger.gz | |||
| SRR7119790_2.fastq.gz | Fastqsanger.gz | |||
| SRR7119800_1.fastq.gz | Fastqsanger.gz | |||
| SRR7119800_2.fastq.gz | Fastqsanger.gz | |||
| SRR7119820.fastq.gz | Fastqsanger.gz |
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Project description:Goal of the experiment was to assess the differences in gene expression between zygotic rnf2 mutant zebrafish embryos and wildtype embryos at 3 dpf. The goal of ChIP-sequencing of wildtype embryos at 3 dpf is to link deregulation in gene expression to the Rnf2 occupancy in the wildtype situation and check the overlap between Rnf2 and H3K27me3. The RNA-sequencing of single hearts was performed to assess differences in gene expression between zygotic rn2 mutants hearts and wildtype hearts at 3 different stages (1, 2, 3 dpf)
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Project description:Polycomb repressive complex PRC1 is essential for gene regulation in numerous cell fate decisions. We show that RING1B (RING2, RNF2) and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer (BC). Moreover, cPRC1 complexes functionally associate with genes regulated by cell type specific key transcription factors such as estrogen receptor (ER) in ER+ tumor cells and BRD4 in triple negative BC cells. cPRC1 is recruited to active enhancers in a manner independent of PRC2 and RING1B enzymatic activity. RING1B regulates enhancer activity and gene transcription not only by promoting the expression of BC oncogenes but also by regulating chromatin accessibility for oncogenic transcription factors. RING1B recruitment, and thus PRC1 association, to active enhancers occurs in multiple cancers.
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Project description:The essential histone variant H2A.Z localises to both active and silent chromatin sites. In embryonic stem cells (ESCs), H2A.Z is also reported to co-localise with polycomb repressive complex 2 (PRC2) at developmentally silenced genes. The mechanism of H2A.Z targeting is not clear, but a role for the PRC2 component Suz12 has been suggested. Given this association, we wished to determine if polycomb functionally directs H2A.Z incorporation in ESCs. We demonstrate that the PRC1 component Ring1B interacts with multiple complexes in ESCs. Moreover, we show that although the genomic distribution of H2A.Z co-localises with PRC2, Ring1B and with the presence of CpG islands, H2A.Z still blankets polycomb target loci in the absence of Suz12, Eed (PRC2) or Ring1B (PRC1). Therefore we conclude that H2A.Z accumulates at developmentally silenced genes in ESCs in a polycomb independent manner.
2012-04-16 | GSE36999 | GEO
Project description:The essential histone variant H2A.Z localises to both active and silent chromatin sites. In embryonic stem cells (ESCs), H2A.Z is also reported to co-localise with polycomb repressive complex 2 (PRC2) at developmentally silenced genes. The mechanism of H2A.Z targeting is not clear, but a role for the PRC2 component Suz12 has been suggested. Given this association, we wished to determine if polycomb functionally directs H2A.Z incorporation in ESCs. We demonstrate that the PRC1 component Ring1B interacts with multiple complexes in ESCs. Moreover, we show that although the genomic distribution of H2A.Z co-localises with PRC2, Ring1B and with the presence of CpG islands, H2A.Z still blankets polycomb target loci in the absence of Suz12, Eed (PRC2) or Ring1B (PRC1). Therefore we conclude that H2A.Z accumulates at developmentally silenced genes in ESCs in a polycomb independent manner. Array design includes 2 biological replicates for all samples and technical replication (dye swaps for H3K27me3_WT_ES, EZH2_WT_ES, EZH2_RING1b_KO_ES, H2AZ_WT_ES(2), H2AZ_Eed_KO_ES and H2AZ_Suz12_KO_ES). Ring1B_WT_ES is represented by a single replicate.
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Project description:Polycomb complexes have traditionally been prescribed roles as transcriptional repressors, though increasing evidence demonstrate they can also activate gene expression. However, the mechanisms underlying positive gene regulation mediated by Polycomb proteins are poorly understood. Here, we show that RING1B, a core component of Polycomb Repressive Complex 1, regulates enhancer-promoter interaction of the bona fide estrogen-activated GREB1 gene. Systematic characterization of RNA:DNA hybrid formation (R-loops), nascent transcription, and RNA Pol II activity upon estrogen administration revealed a key role of RING1B in gene activation by regulating R-loop formation and RNA Pol II elongation. We also found that the estrogen receptor (ER) and RNA are both necessary for full RING1B recruitment to estrogen-activated genes. Notably, RING1B recruitment was mostly unaffected upon RNA Pol II depletion by triptolide. Our findings delineate the functional interplay between RING1B, RNA, and ER to safeguard chromatin architecture perturbations required for estrogen-mediated gene regulation, and highlight the crosstalk between steroid hormones and Polycomb proteins to regulate oncogenic programs.
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Project description:Genome-wide distribution of proteins and histone marks in CD43 negative mouse resting B cells ChIP-seq analyses of Aurora B, Ring1B, Bcx7, USP16, H3K27me3, and Ezh2 were carried out on wild-typeCD43 negative resting B cells. ChIP-seq datasets obtained from Aurora B knockout and RingiB knockout cells were used as negative controls to validate the signals for Aurora B and Ring1B from wild-type cells. 8WG16 ChIP-seq datasets were generated from WT (Cre-ERt2 homozygous) and Ring1B KO (Cre-ERt2/Rnf2 flox homozygous). RNAP-S5ph ChIP-seq datasets were generated from WT (Cre-ERt2 homozygous) and Aurkb KO (Cre-ERt2/Aurkb flox homozygous). ChIP-seq analyses of H3S28 phosphorylation (H3S28ph) and H2AK119 monoubiquitination (H2Aub1) in wild-type (Cre-ERt2 homozygous) and Aurora B KO (Cre-ERt2/Aurkb flox homozygous) CD43 negative resting B cells treated with 250nM tamoxifen (4-hydroxytamoxifen) for 48 hours. ChIP-seq analyses of the levels of unphosphorylated RNA Pol II (8WG16) and serine 5-phosphorylated RNA Pol II (RNAP-S5ph) were conducted in Aurkb KO (Cre-ERt2/Aurkb flox homozygous) and Ring1B KO (Cre-ERt2/Rnf2 flox homozygous) CD43 negative resting B cells treated with 250nM tamoxifen (4-hydroxytamoxifen) for 48 hours respectively). All libraries were prepared from sonicated, formaldehyde-crossilinked chromatin. For H2Aub1, ChIP was performed using micrococcal nuclease-digested, unfixed chromatin, instead.
2013-09-27 | E-GEOD-42705 | biostudies-arrayexpress
Project description:NguyenLK2011 - Ubiquitination dynamics in
Ring1B-Bmi1 system
This theoretical model investigates the
dynamics of Ring1B/Bmi1 ubiquitination to identify bistable
switch-like and oscillatory behaviour in the
system. Michaelis-Menten (MM) equations are used to formulate
the model. However, the authors show that the dynamics persist even
for Mass-Action kinetics. This SBML file is the MM version of the
model.
This model is described in the article:
Switches,
excitable responses and oscillations in the Ring1B/Bmi1
ubiquitination system.
Nguyen LK, Muñoz-García J,
Maccario H, Ciechanover A, Kolch W, Kholodenko BN.
PLoS Comput. Biol. 2011 Dec; 7(12):
e1002317
Abstract:
In an active, self-ubiquitinated state, the Ring1B ligase
monoubiquitinates histone H2A playing a critical role in
Polycomb-mediated gene silencing. Following ubiquitination by
external ligases, Ring1B is targeted for proteosomal
degradation. Using biochemical data and computational modeling,
we show that the Ring1B ligase can exhibit abrupt switches,
overshoot transitions and self-perpetuating oscillations
between its distinct ubiquitination and activity states. These
different Ring1B states display canonical or multiply branched,
atypical polyubiquitin chains and involve association with the
Polycomb-group protein Bmi1. Bistable switches and oscillations
may lead to all-or-none histone H2A monoubiquitination rates
and result in discrete periods of gene (in)activity. Switches,
overshoots and oscillations in Ring1B catalytic activity and
proteosomal degradation are controlled by the abundances of
Bmi1 and Ring1B, and the activities and abundances of external
ligases and deubiquitinases, such as E6-AP and USP7.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000622.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000622 | BioModels
Project description:The Polycomb repressive complexes PRC1 and PRC2 play an essential role in cell fate decisions, embryonic development and gene regulation. While the functions of PRC2 in cancer are under intense study, the function of PRC1 in cancer remains largely unexplored. Here, we show that RNF2, the gene encoding RING1B, and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer. Specifically, in estrogen receptor positive (ER+) breast cancer cells, cPRC1 is functionally associated with enhancers and genes regulated by ERa, while in triple negative breast cancer (TNBC) cells, a different cPRC1 variant is recruited to enhancers and promoters occupied by the bromodomain protein BRD4. Mechanistically, cPRC1 complexes are recruited to active enhancers independently of PRC2 and RING1B enzymatic activity. Moreover, RING1B has a dual role in regulating enhancer activity and gene transcription as it is recruited to enhancers to maintain and promote gene expression of breast cancer oncogenes. We also show that RING1B regulates chromatin accessibility of oncogenic transcription factors. Finally, we provide evidence that association of PRC1 to active enhancers is not restricted to breast cancer, demonstrating that RING1B recruitment to transcriptionally active sites occurs in multiple cancer types. Our work highlights a non-classical function of cPRC1 complexes in regulating specific oncogenic programs in cancer through its association with enhancer regions.
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Project description:In mammals, totipotent pre-implantation embryos are formed by fusion of highly differentiated oocytes and spermatozoa. Acquisition of totipotency concurs with remodeling of chromatin states of parental genomes (M-bM-^@M-^\epigenetic reprogrammingM-bM-^@M-^]), changes in maternally contributed transcriptome and proteome, and zygotic genome activation. Genomes of mature germ cells are more proficient in supporting embryonic development than those of somatic cells. It is currently unknown whether transgenerational inheritance of chromatin states present in mature gametes underlies the efficacy of early embryonic development after natural conception. Here, we show that Ring1 and Rnf2, two core components of the Polycomb Repressive Complex 1 (PRC1), serve redundant gene regulatory functions during oogenesis that are required to support embryonic development beyond the two-cell stage. Numerous developmental regulatory genes that are established Polycomb targets in various somatic cell types are de-repressed in Ring1/Rnf2 double mutant (dm) fully grown germinal vesicle (GV) oocytes. Translation of tested aberrant maternal transcripts is, however, delayed until after fertilization. Exchange of maternal pro-nuclei between control and Ring1/Rnf2 maternally dm early zygotes demonstrates an essential role for Ring1 and Rnf2 during oogenesis in defining cytoplasmic and nuclear maternal contributions that are both essential for proper initiation of embryonic development. A large number of genes up-regulated in Ring1/Rnf2 dm GV oocytes harbor PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) in spermatozoa and in embryonic stem cells (ESCs), and are repressed during normal oogenesis and early embryogenesis. These data strongly support the model that Polycomb acts in the female and male germline to silence differentiation inducing genes and to program chromatin states, thereby sustaining developmental potential across generations. Expression profiling of fully grown mouse GV oocytes was performed with the following genotypes: Ring1+/+Rnf2F/F (control), Ring1-/-Rnf2F/F (Ring1 mutant), Ring1+/+Rnf2F/FZp3-cre (Rnf2 mutant) and Ring1-/-Rnf2F/FZp3-cre (Ring1/Rnf2 double mutant). 12 samples were analyzed: 3 biological replicates of each of the 4 genotypes (Ring1+/+Rnf2F/F (control), Ring1-/-Rnf2F/F (Ring1 mutant), Ring1+/+Rnf2F/FZp3-cre (Rnf2 mutant) and Ring1-/-Rnf2F/FZp3-cre (Ring1/Rnf2 double mutant)). Each sample contains 50 GV oocytes.
2012-05-06 | E-GEOD-23033 | biostudies-arrayexpress