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ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells

ABSTRACT: We have performed ChIP seq analysis to obtain the positions of KAP1 and ZFP57 binding sites in mouse ES cells. By comparing the two lists, we were able to find bona fide sites. ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells

ORGANISM(S): Mus musculus

SUBMITTER: Simon Quenneville

PROVIDER: E-GEOD-31181 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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In embryonic stem cells, ZFP57/KAP1 recognize a methylated hexanucleotide to affect chromatin and DNA methylation of imprinting control regions.

Quenneville Simon S Verde Gaetano G Corsinotti Andrea A Kapopoulou Adamandia A Jakobsson Johan J Offner Sandra S Baglivo Ilaria I Pedone Paolo V PV Grimaldi Giovanna G Riccio Andrea A Trono Didier D

Molecular cell 20111101 3

The maintenance of H3K9 and DNA methylation at imprinting control regions (ICRs) during early embryogenesis is key to the regulation of imprinted genes. Here, we reveal that ZFP57, its cofactor KAP1, and associated effectors bind selectively to the H3K9me3-bearing, DNA-methylated allele of ICRs in ES cells. KAP1 deletion induces a loss of heterochromatin marks at ICRs, whereas deleting ZFP57 or DNMTs leads to ICR DNA demethylation. Accordingly, we find that ZFP57 and KAP1 associated with DNMTs a ...[more]

PMID: 22055183

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ZFP57/KAP1 recognize a methylated hexanucleotide to affect the chromatin and DNA methylation of imprinting control regions in embryonic stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE31181: ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells GSE31182: RNA-seq and expression profile of WT and ZFP57 KO ES cells Refer to individual Series

2011-11-07 | E-GEOD-31183 | biostudies-arrayexpress

ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells

Project description:We have performed ChIP seq analysis to obtain the positions of KAP1 and ZFP57 binding sites in mouse ES cells. By comparing the two lists, we were able to find bona fide sites.

2011-11-07 | GSE31181 | GEO

ChIP-seq analysis of KAP1 and H3K9me3 modifications in mouse spleen B cells

Project description:Chromatin remodeling is fundamental for B cell differentiation. Here, we explored the role in this process of KAP1, the cofactor of KRAB-ZFP transcriptional repressors. B lymphoid-specific Kap1 knockout mice displayed reduced numbers of mature B cells, lower steady-state levels of antibodies and accelerated rates of decay of neutralizing antibodies following viral immunization. Transcriptome analyses of Kap1-deleted B splenocytes revealed an upregulation of PTEN, the enzymatic counter-actor of PIK3 signaling, and of genes encoding DNA damage response factors, cell-cycle regulators and chemokine receptors. ChIP/seq studies established that KAP1 bound at or close to a number of these genes, and controlled chromatin status at their promoters. Genome-wide, KAP1-binding sites avoided active B cell-specific enhancers and were enriched in repressive histone marks, further supporting a role for this molecule in gene silencing in vivo. Likely responsible for tethering KAP1 to at least some of these targets, a discrete subset of KRAB-ZFPs is enriched in B lymphocytes. This work thus reveals the role of KRAB/KAP1-mediated epigenetic regulation in B cell development and homeostasis. Examination of KAP1 binding sites and H3K9me3 enriched regions in KAP1 wild type and KO mouse B splenocytes.

2012-05-16 | E-GEOD-36850 | biostudies-arrayexpress

ChIP-seq analysis of KAP1 binding and H3K9me3 modifications in mouse T cell progenitors

Project description:Chromatin remodelling at specific genomic loci controls lymphoid differentiation. Here, we investigated the role played in this process by Kruppel-Associated Box (KRAB)- Associated Protein 1 (KAP1), the universal cofactor of KRAB-zinc finger proteins (-ZFPs), a tetrapod-restricted family of transcriptional repressors. T cell-specific Kap1-deleted mice displayed a significant expansion of immature thymocytes, imbalances in CD4+/CD8+ cell ratios and impaired responses to TCR stimulation when compared to littermate KAP1 control mice. Transcriptome and chromatin studies revealed that KAP1 binds T cell-specific cis-acting regulatory elements marked by the H3K9me3 repressive mark and enriched in Ikaros/NuRD complexes. Also, KAP1 directly controls the expression of several genes involved in TCR and cytokine signalling. Among these, regulation of FoxO1 seems to play a major role in this system. Likely responsible for tethering KAP1 to at least part of its genomic targets, a small number of KRAB-ZFPs are selectively expressed in T lymphoid cells. These results reveal the so-far unsuspected yet important role of KAP1-mediated epigenetic regulation in T lymphocyte differentiation and activation. Examination of KAP1 binding sites and H3K9me3-enriched regions in wild type and KAP1 KO mouse thymocytes.

2012-12-16 | E-GEOD-38579 | biostudies-arrayexpress

KAP1 regulates gene networks controlling B lymphoid cell differentiation and function

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2012-05-16 | E-GEOD-36880 | biostudies-arrayexpress

KAP1 regulates gene networks controlling T cell development and activation

Project description:This SuperSeries is composed of the following subset Series: GSE34447: Gene expression analysis of wild type and KAP1 KO mouse T cell progenitors GSE38579: ChIP-seq analysis of KAP1 binding and H3K9me3 modifications in mouse T cell progenitors Refer to individual Series

2012-08-07 | E-GEOD-38580 | biostudies-arrayexpress

RNA-seq and expression profile of WT and ZFP57 KO ES cells

Project description:RNA-seq and expression profile of WT and ZFP57 KO ES cells RNA was extracted from both cell lines, PolyA RNA were extracted and RNA-seq was performed

2011-11-07 | E-GEOD-31182 | biostudies-arrayexpress

ZFP57 recognizes multiple and closely spaced sequence motif variants to maintain repressive epigenetic marks in mouse embryonic stem cells

Project description:In mouse embryonic stem cells SNPs disrupting closely-spaced hexanucleotide motifs are associated with lack of ZFP57 binding and H3K9me3 enrichment. Examination of ZFP57-KAP1 allele-specific binding in two lines of mouse embryonic stem cells JB1 and BJ1 generated from F1 hybrids derived from JF1 x B6 and B6 x JF1 crosses respectively.

2015-11-06 | E-GEOD-74757 | biostudies-arrayexpress

Epigenetic regulation of unique genes and repetitive elements by KRAB zinc finger protein ZFP57 in embryonic stem cells

Project description:KRAB-zinc finger proteins (KZFPs) represent one of the largest families of DNA binding proteins in vertebrate genomes and appear to have evolved to silence transposable elements (TEs) including endogenous retroviruses through sequence-specific targeting of repressive chromatin states. However, one member, ZFP57, is required to maintain the post-fertilization DNA methylation memory of parental-origin at genomic imprints. We have conducted RNA-seq and ChIP-seq analyses in normal and ZFP57 mutant ES cells to characterize the targets of ZFP57 in more detail. Over 80% of ZFP57 targets are TEs. However, mutants indicate that ZFP57 is not essential for their repression in ES cells. The remaining targets lie within unique imprinted and non-imprinted sequences. Though loss of ZFP57 influences imprinted genes as expected, the majority of unique gene targets lose H3K9me3 with little effect on DNA methylation and with very few exhibiting alterations in expression. Furthermore, comparison with DNA methyltransferase-deleted ES cells (TKO) identifies remarkably similar losses of H3K9me3 and changes in expression, defining regions where H3K9me3 is secondary to DNA methylation. We determine that ZFP57 is the principal methylation-sensitive KZFP recruiting KAP1 and H3K9me3 in ES cells. Finally, like imprints, other unique targets of ZFP57 are enriched for germline-derived DNA methylation including oocyte-specific methylation that is resistant to post-fertilisation epigenetic reprogramming. Our analyses suggest the evolution of a DNA methylation sensitive KZFP, that may serve to reinforce the silenced state at TEs, but whose primary function is to maintain DNA methylation and repressive histone marks at imprinted regions.

2019-08-21 | GSE123942 | GEO

The intracellular mediators of the BMP pathway SMAD1/5 bind the Imprinting Control Regions through interaction with the ZFP57/KAP1 complex and contribute to maintain their DNA methylation and H3K9me3 in mouse embryonic stem cells

Project description:We report that SMAD1/5 bind the ICRs by interacting with the ZFP57/KAP1 complex and that this is necessary for the proper maintenance of methylation imprints in mESCs

2017-12-07 | GSE90985 | GEO

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