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The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE42706 | GEO | 2013/09/27

SECONDARY ACCESSION(S): PRJNA182901

REPOSITORIES: GEO

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The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-09-27 | E-GEOD-42706 | biostudies-arrayexpress

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [ChIP-seq]

Project description:Genome-wide distribution of proteins and histone marks in CD43 negative mouse resting B cells

2013-09-27 | GSE42705 | GEO

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [RNA-Seq]

Project description:Expression profiling of resting B cells to classify active and silent genes based on expression levels

2013-09-27 | GSE42704 | GEO

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [RNA-Seq]

Project description:Expression profiling of resting B cells to classify active and silent genes based on expression levels 4 biological replicates of mRNA extracted from freshly purified mouse CD43 negative resting B cells

2013-09-27 | E-GEOD-42704 | biostudies-arrayexpress

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [ChIP-seq]

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

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes

Project description:The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes

| PRJNA182901 | ENA

Polycomb Group Proteins RING1A and RING1B Regulate the Vegetative Phase Transition in <i>Arabidopsis</i>.

Project description:Polycomb group (PcG) protein-mediated gene silencing is a major regulatory mechanism in higher eukaryotes that affects gene expression at the transcriptional level. Here, we report that two conserved homologous PcG proteins, RING1A and RING1B (RING1A/B), are required for global H2A monoubiquitination (H2Aub) in Arabidopsis. The mutation of RING1A/B increased the expression of members of the SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) gene family and caused an early vegetative phase transition. The early vegetative phase transition observed in ring1a ring1b double mutant plants was dependent on an SPL family gene, and the H2Aub status of the chromatin at SPL locus was dependent on RING1A/B. Moreover, mutation in RING1A/B affected the miRNA156a-mediated vegetative phase transition, and RING1A/B and the AGO7-miR390-TAS3 pathway were found to additively regulate this transition in Arabidopsis. Together, our results demonstrate that RING1A/B regulates the vegetative phase transition in Arabidopsis through the repression of SPL family genes.

| S-EPMC5443144 | biostudies-literature

Polycomb group targeting through different binding partners of RING1B C-terminal domain.

Project description:RING1B, a Polycomb Group (PcG) protein, binds methylated chromatin through its association with another PcG protein called Polycomb (Pc). However, RING1B can associate with nonmethylated chromatin suggesting an alternate mechanism for RING1B interaction with chromatin. Here, we demonstrate that two proteins with little sequence identity between them, the Pc cbox domain and RYBP, bind the same surface on the C-terminal domain of RING1B (C-RING1B). Pc cbox and RYBP each fold into a nearly identical, intermolecular beta sheet with C-RING1B and a loop structure which are completely different in the two proteins. Both the beta sheet and loop are required for stable binding and transcription repression. Further, a mutation engineered to disrupt binding on the Drosophila dRING1 protein prevents chromatin association and PcG function in vivo. These results suggest that PcG targeting to different chromatin locations relies, in part, on binding partners of C-RING1B that are diverse in sequence and structure.

| S-EPMC4445678 | biostudies-literature

The polycomb group protein ring1b/rnf2 is specifically required for craniofacial development.

Project description:Polycomb group (PcG) genes are chromatin modifiers that mediate epigenetic silencing of target genes. PcG-mediated epigenetic silencing is implicated in embryonic development, stem cell plasticity, cell fate maintenance, cellular differentiation and cancer. However, analysis of the roles of PcG proteins in maintaining differentiation programs during vertebrate embryogenesis has been hampered due to the early embryonic lethality of several PcG knock-outs in the mouse. Here, we show that zebrafish Ring1b/Rnf2, the single E3 ubiquitin ligase in the Polycomb Repressive Complex 1, critically regulates the developmental program of craniofacial cell lineages. Zebrafish ring1b mutants display a severe craniofacial phenotype, which includes an almost complete absence of all cranial cartilage, bone and musculature. We show that Cranial Neural Crest (CNC)-derived cartilage precursors migrate correctly into the pharyngeal arches, but fail to differentiate into chondrocytes. This phenotype is specific for cartilage precursors, since other neural crest-derived cell lineages, including glia, neurons and chromatophores, are formed normally in ring1b mutants. Our results therefore reveal a critical and specific role for Ring1b in promoting the differentiation of cranial neural crest cells into chondrocytes. The molecular mechanisms underlying the pathogenesis of craniofacial abnormalities, which are among the most common genetic birth defects in humans, remain poorly understood. The zebrafish ring1b mutant provides a molecular model for investigating these mechanisms and may lead to the discovery of new treatments or preventions of craniofacial abnormalities.

| S-EPMC3770662 | biostudies-literature

Aurora A kinase phosphorylates Hec1 to regulate metaphase kinetochore-microtubule dynamics.

Project description:Precise regulation of kinetochore-microtubule attachments is essential for successful chromosome segregation. Central to this regulation is Aurora B kinase, which phosphorylates kinetochore substrates to promote microtubule turnover. A critical target of Aurora B is the N-terminal "tail" domain of Hec1, which is a component of the NDC80 complex, a force-transducing link between kinetochores and microtubules. Although Aurora B is regarded as the "master regulator" of kinetochore-microtubule attachment, other mitotic kinases likely contribute to Hec1 phosphorylation. In this study, we demonstrate that Aurora A kinase regulates kinetochore-microtubule dynamics of metaphase chromosomes, and we identify Hec1 S69, a previously uncharacterized phosphorylation target site in the Hec1 tail, as a critical Aurora A substrate for this regulation. Additionally, we demonstrate that Aurora A kinase associates with inner centromere protein (INCENP) during mitosis and that INCENP is competent to drive accumulation of the kinase to the centromere region of mitotic chromosomes. These findings reveal that both Aurora A and B contribute to kinetochore-microtubule attachment dynamics, and they uncover an unexpected role for Aurora A in late mitosis.

| S-EPMC5748988 | biostudies-literature

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