Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA154073 | ENA |
REPOSITORIES: ENA
Similar Datasets
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. ChIP-Seq of HA tagged ZFP57 and KAP1 in mouse ES cells
2011-11-07 | E-GEOD-31181 | biostudies-arrayexpress
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
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
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
Project description:Nr5a2 (also known as liver receptor homolog-1, Lrh-1) has been shown to bind both the proximal enhancer and proximal promoter regions of Pou5f1 and regulate Pou5f1 in the epiblast stage of mouse embryonic development (Gu et al., 2005). Nr5a2-null embryos display a loss of Oct4 expression in the epiblasts (Gu et al., 2005) and die between E6.5 and E7.5 (Gu et al., 2005; Pare et al., 2004). To identify the targets of Nr5a2, we generated a stable ES cell-line that expresses HA-tagged Nr5a2. Anti-HA antibody was used to immunoprecipitate HA-Nr5a2 for ChIP-seq analysis. Keywords: Transcription factor binding sites To identify the binding sites of Nr5a2, we generated a stable ES cell-line that expresses HA-tagged Nr5a2. Anti-HA antibody was used to immunoprecipitate HA-Nr5a2.
2010-01-22 | E-GEOD-19019 | biostudies-arrayexpress
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
Project description:We show that a hitherto poorly characterized KRAB domain-containing zinc-finger (ZF) transcription factor, ZFP30, positively regulates adipogenesis. We demonstrate ZFP30’s function in murine in vitro and in vivo models, as well as in human stromal vascular fraction cells. We reveal through mechanistic studies that ZFP30 directly targets and activates Pparg2 by binding a retrotransposon-derived enhancer, suggesting a process of adipogenic exaptation. We further show that ZFP30 recruits the co-regulator KRAB-associated protein 1 (KAP1), which, surprisingly, acts as a ZFP30 co-activator in this adipogenic context. As neither the commercial ZFP30 antibodies nor four batches of customized ZFP30 antibodies recognized it specifically (data not shown), we performed ChIP-seq in 3T3-L1 cells expressing HA-tagged ZFP30 in a tetracycline-inducible manner, as also previously employed for ZEB1 (Gubelmann et al., 2014). The mRNA expression of exogenous Zfp30 was induced to a similar level as the endogenous Zfp30 by adjusting the amount of Doxycycline (data not shown), to avoid potential artefacts due to protein overexpression. To further characterize its role in adipogenesis and as a ZFP30 partner, we performed KAP1 ChIP-seq in undifferentiated (day 0) and differentiated (day 2) 3T3-L1 cells, as described above for HA-ZFP30. We first confirmed the high enrichment obtained with the employed KAP1 antibody.
2019-03-01 | E-MTAB-6817 | biostudies-arrayexpress
Project description:Nr5a2 (also known as liver receptor homolog-1, Lrh-1) has been shown to bind both the proximal enhancer and proximal promoter regions of Pou5f1 and regulate Pou5f1 in the epiblast stage of mouse embryonic development (Gu et al., 2005). Nr5a2-null embryos display a loss of Oct4 expression in the epiblasts (Gu et al., 2005) and die between E6.5 and E7.5 (Gu et al., 2005; Pare et al., 2004). To identify the targets of Nr5a2, we generated a stable ES cell-line that expresses HA-tagged Nr5a2. Anti-HA antibody was used to immunoprecipitate HA-Nr5a2 for ChIP-seq analysis. Keywords: Transcription factor binding sites
2010-01-22 | GSE19019 | GEO
Project description:Selective maintenance of genomic methylation imprints during pre-implantation development is required for parental origin-specific expression of imprinted genes. The Kruppel-like zinc finger protein ZFP57 acts as a factor necessary for maintaining the DNA methylation memory at multiple imprinting control regions (ICRs) in early mouse embryos and ES cells. Maternal-zygotic deletion of ZFP57 in mice presents a highly penetrant phenotype with no animals surviving to birth. In addition, several cases of human transient neonatal diabetes (TND) are associated with somatic mutations in ZFP57 coding sequence. Here we comprehensively map sequence-specific ZFP57 binding sites in an allele-specific manner using hybrid ES cell lines from reciprocal crosses between C57BL/6J and Cast/EiJ mice assigning allele specificity to approximately two thirds of all binding sites. While half of these are biallelic and include ERV targets, the rest show mono-allelic binding based either on parental-origin or on genetic background of the allele. Parental-origin allele-specific binding was methylation-dependent and mapped only to imprinted DMRs established in the germline (gDMRs). No binding was evident at secondary somatically-derived DMRs. ZFP57-bound gDMRs can predict imprinted gene expression and we identify new imprinted genes, including the Fkbp6 gene with a critical function in mouse male germ cell development. Genetic-background specific sequence differences also influence ZFP57 binding. We show that genetic variation that disrupts the consensus binding motif and its methylation is associated with mono-allelic expression of neighbouring genes. The work described here uncovers further roles for ZFP57 mediated regulation of genomic imprinting and identifies a novel mechanism for genetically determined mono-allelic gene expression. Input and Zfp57 CHiP-Seq profiles of hybrid Black6/Cast ES cells were generated by sequencing using the Illumina GAIIx platform.
2015-05-08 | E-GEOD-55382 | biostudies-arrayexpress
Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected. HA-tagged Gm6871 ChIP-seq in mES cells, RNA-seq in control and Gm6871 KD mES cells, KAP1 ChIP-seq in WT mES cells, RNA-seq in control and DNMTs KD hES cells.
2014-06-09 | E-GEOD-58323 | biostudies-arrayexpress