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Phf19 links methylated lysine 36 of histone H3 to regulation of Polycomb activity

ABSTRACT: Gene expression profile in control (shCTR) and Phf19 depleted (sh4) mouse embryonic stem cell untreated or treated 72 hr with 1 M-NM-

ORGANISM(S): Mus musculus

SUBMITTER: Luciano Di Croce

PROVIDER: E-GEOD-41277 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Phf19 links methylated lysine 36 of histone H3 to regulation of Polycomb activity

Project description:Gene expression profile in control (shCTR) and Phf19 depleted (sh4) mouse embryonic stem cell untreated or treated 72 hr with 1 μM retinoic acid (72 RA).

2012-10-04 | GSE41277 | GEO

Phf19 links methylated lysine 36 of histone H3 to regulation of Polycomb activity [ChIP-Seq]

Project description:Polycomb group proteins are transcriptional repressors that play essential roles in regulating genes required for differentiation and embryonic development. The Polycomb repressive complex 2 (PRC2) contains the methyltransferase activity for lysine 27 on histone 3 (H3K27me3), which is a docking site for the PRC1 complex and leads to gene repression. However, the role of other histone modifications in regulating PRC2 activity is just beginning to be understood. Here we show that direct recognition of histone H3 methylated at lysine 36 (H3K36me), an mark associated with activation, by the PRC2 subunit Phf19 is required for the full enzymatic activity of the PRC2 complex. We provide structural evidence for this interaction by nuclear magnetic resonance spectroscopy (NMR). Using genome-wide chromatin binding analyses and expression analyses, we show that Phf19 binds to a subset of PRC2 targets in embryonic stem (ES) cells, and that this is required for their repression and for H3K27me3 deposition. These findings reveal that the H3K36me2/3-Phf19 interaction is essential for PRC2 complex activity and for proper regulation of gene repression in ES cells. We determined the genome binding/occupancy profile of Phf19, H3K36me3, H3K36me2, H3K27me3 and Suz12 by high throughput sequencing in mouse embryonic stem cells. For Phf19 two independent biological replicas were performed and Phf19 binding sites were defined as those sites (ChIP-seq peaks) present in both replicas. H3K27me3 was evaluated in control ES cells and cells depleted of Phf19 (shRd and shPhf19 respectively).

2012-10-16 | E-GEOD-41589 | biostudies-arrayexpress

Phf19 knockdown effect on F9 embryonal carcinoma cells

Project description:PCL family protein Phf19/Pcl3 is one of the accessory components of the PRC2 core complex, and Phf19 is highly expressed in murine ES cells and an ES cell-like embryonic carcinoma cell line, F9 cells. Here we performed microarray analysis of embryonal carcinoma cell line F9 following Phf19 knockdown by shRNA. Knocking down Phf19/Pcl3 in F9 embryonic cells led to derepression of numerous PRC2 direct target genes. 4 sampels including 2 shRNA vector control cell lines and 2 shPhf19 cell lines were used for RNA extraction and Affymetrix mouse 430 2.0 arrays.

2012-12-20 | E-GEOD-42463 | biostudies-arrayexpress

Phf19 knockdown effect on F9 embryonal carcinoma cells

2012-12-20 | GSE42463 | GEO

PHF19 mediated regulation of proliferation and invasiveness in prostate cancer

Project description:The Polycomb-like protein PHF19/PCL3 associates with the Polycomb repressive complex 2 (PRC2) and mediates its recruitment to chromatin in embryonic stem cells, where it is essential for maintaining the repression of developmental genes. PHF19 is also overexpressed in many cancers. However, neither PHF19 targets in cancer cells nor potentially misregulated pathways involving PHF19 are known. Here, we investigate the role of PHF19 in prostate cancer cells. We find that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin. Direct PHF19 target genes are involved in proliferation, differentiation, angiogenesis, and extracellular matrix organization, among others. Depletion of PHF19 triggers an increase in MTF2/PCL2 recruitment to chromatin, along with a genome-wide gain in PRC2 occupancy and H3K27me3 deposition. Transcriptome analysis shows that loss of PHF19 promotes deregulation of key genes involved in growth, metastasis, and invasion, as well as of factors that stimulate formation of new blood vessels. Consistent with this, PHF19 silencing reduces cell proliferation rate and promotes invasive growth and angiogenesis. Taking together, our findings reveal a role for PHF19 in controlling the balance between cell proliferation and invasiveness in prostate cancer.

2020-03-16 | GSE135623 | GEO

PHF19 isoforms induced gene expression alteration in colon cancer cells

Project description:This experiment is designed to evaluate gene expression alteration following silencing PHF19 isoforms in colon cancer cells. Total RNA were extraced from indicated stable cell lines, two biological replications for each treatment.

2014-03-22 | E-GEOD-52019 | biostudies-arrayexpress

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (ChIP-seq)

Project description:We here report a PRC2-associated cofactor, PHD finger protein 19 (PHF19, also known as Polycomb-like 3), as a crucial mediator of tumorigenicity in multiple myeloma (MM). Using various MM models, we demonstrated a critical requirement of PHF19 for tumor growth in vitro and in vivo. Mechanistically, PHF19-mediated oncogenic effect relies on its PRC2-interacting and chromatin-binding functions. ChIP-Seq profiling showed a critical role for PHF19 in maintaining the H3K27me3 landscape. PHF19 depletion led to loss of broad H3K27me3 domains possibly due to impaired H3K27me3 spreading from CpG islands

2019-08-31 | GSE135890 | GEO

Effect of overexpression of PHF19 in multiple myeloma cells [RNA-seq]

Project description:To investigate the transcriptomic effect of PHF19 overexpression in MM cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of AMO1 cells with differential PHF19 expression.

2023-01-31 | GSE224200 | GEO

Phf19 links methylated lysine 36 of histone H3 to regulation of Polycomb activity [ChIP-Seq]

2012-10-16 | GSE41589 | GEO

Knockdown and Overexpression of Cbx4 wild type, Cbx4 chromodomain mutant, and Cbx4 sumoylation mutant in human epidermal stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE31093: Knockdown and Overexpression of Cbx4 wild type and of a Cbx4 chromodomain mutant in human epidermal stem cells GSE31094: Overexpression of Cbx4 wild type and of a Cbx4 sumoylation mutant in human epidermal stem cells Refer to individual Series

2011-08-02 | E-GEOD-31147 | biostudies-arrayexpress

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