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Polycomb proteins link Proliferation with DNA Replication

ABSTRACT: Polycomb proteins control proliferation and cellular transformation regulating DNA replication independently of cell cycle checkpoints

ORGANISM(S): Mus musculus

PROVIDER: GSE48520 | GEO | 2014/04/15

SECONDARY ACCESSION(S): PRJNA210421

REPOSITORIES: GEO

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Polycomb proteins link Proliferation with DNA Replication

Project description:Polycomb proteins control proliferation and cellular transformation regulating DNA replication independently of cell cycle checkpoints Total RNA was extracted from MEF cells (derived from Ola129 mice) transiently transfected with Ezh2 specific and control esiRNA oligos 48 hrs. post-transfection.

2014-04-15 | E-GEOD-48520 | biostudies-arrayexpress

Polycomb-like proteins link the PRC2 complex to CpG islands

Project description:The Polycomb repressive complex 2 (PRC2) mainly mediates transcriptional repression and has essential roles in various biological processes including the maintenance of cell identity and proper differentiation. Polycomb-like (PCL) proteins, such as PHF1, MTF2 and PHF19, are PRC2-associated factors that form sub-complexes with PRC2 core components, and have been proposed to modulate the enzymatic activity of PRC2 or the recruitment of PRC2 to specific genomic loci. Mammalian PRC2-binding sites are enriched in CG content, which correlates with CpG islands that display a low level of DNA methylation. However, the mechanism of PRC2 recruitment to CpG islands is not fully understood. Here we solve the crystal structures of the N-terminal domains of PHF1 and MTF2 with bound CpG-containing DNAs in the presence of H3K36me3-containing histone peptides. We show that the extended homologous regions of both proteins fold into a winged-helix structure, which specifically binds to the unmethylated CpG motif but in a completely different manner from the canonical winged-helix DNA recognition motif. We also show that the PCL extended homologous domains are required for efficient recruitment of PRC2 to CpG island-containing promoters in mouse embryonic stem cells. Our research provides the first, to our knowledge, direct evidence to demonstrate that PCL proteins are crucial for PRC2 recruitment to CpG islands, and further clarifies the roles of these proteins in transcriptional regulation in vivo.

2017-09-06 | GSE97805 | GEO

Oncogenic Herpesvirus utilizes stress-induced cell cycle checkpoints for efficient lytic replication.

Project description:ChIP-sequencing reads from Oncogenic Herpesvirus utilizes stress-induced cell cycle checkpoints for efficient lytic replication, accepted to PLOS Pathogens

2016-06-01 | E-MTAB-4356 | biostudies-arrayexpress

Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication.

Project description: Not available

| S-EPMC3996544 | biostudies-literature

The TRESLIN-MTBP complex couples completion of DNA replication with S/G2 transition

Project description:It has been proposed that ATR kinase senses the completion of DNA replication to initiate the S/G2 transition. In contrast to this model, we show here that the TRESLIN-MTBP complex prevents a premature entry into G2 from early S-phase independently of ATR/CHK1 kinases. TRESLIN-MTBP acts transiently at pre-replication complexes (preRCs) to initiate origin firing and is released after the subsequent recruitment of CDC45. This dynamic behavior of TRESLIN-MTBP implements a monitoring system that checks the activation of replication forks and senses the rate of origin firing to prevent the entry into G2. This system detects the decline in the number of origins of replication that naturally occurs in very late S, which is the signature that cells use to determine the completion of DNA replication and permit the S/G2 transition. Our work introduces TRESLIN-MTBP as a key player in cell cycle control independent of canonical checkpoints.

2023-03-11 | PXD035353 | Pride

DNA replication-coupled histone modification maintains Polycomb gene silencing in plants

Project description:DNA replication-coupled histone modification maintains Polycomb gene silencing in plants

| PRJNA393888 | ENA

The TRESLIN-MTBP complex couples completion of DNA replication with S/G2 transition

2022-08-06 | GSE210129 | GEO

Polycomb-like proteins link the PRC2 complex to CpG islands.

Project description: Not available

| S-EPMC5937281 | biostudies-literature

SLFN11 blocks stressed replication forks independently of ATR

Project description:SLFN11 blocks stressed replication forks independently of ATR

| PRJNA394710 | ENA

Mechanism and function of DNA replication-independent DNA-protein crosslink repair via the SUMO pathway

Project description:DNA-protein crosslinks (DPCs) obstruct essential DNA transactions, posing a serious threat to genome stability and functionality. DPCs are proteolytically processed in a ubiquitin- and DNA replication-dependent manner by SPRTN or the proteasome but can also be resolved via targeted SUMOylation. However, the mechanistic basis of SUMO-mediated DPC resolution and its interplay with replication-coupled DPC repair pathways remain unknown. Here, we show that the SUMO-targeted ubiquitin ligase RNF4 defines a major pathway for ubiquitylation and proteasomal clearance of SUMOylated DPCs in a DNA replication-independent manner. In addition, we provide evidence that a subset of DPCs can be SUMOylated and processed via transcription, independently of RNF4. SUMO modification of DPCs is mediated by PIAS4 and neither stimulates nor inhibits their rapid DNA replication-dependent proteolysis. Instead, SUMOylation provides a critical salvage mechanism to remove DPCs formed or persisting after replication, as we demonstrate that DPCs on duplex DNA do not activate interphase DNA damage checkpoints. Consequently, in the absence of the SUMO-RNF4 pathway cells can enter mitosis with a high load of unresolved DPCs, leading to defective chromosome segregation and cell death. Collectively, these findings provide mechanistic insights into SUMO-driven pathways underlying replication-independent DPC resolution and highlight their critical importance in maintaining chromosome stability and cellular fitness.

2021-08-06 | PXD021947 | Pride

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