Genome-wide maps of CFP1, RNA Polymerase II and H3K4me3 in mouse brain.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE18578 | GEO | 2010/04/15
SECONDARY ACCESSION(S): PRJNA120285
REPOSITORIES: GEO
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Project description:We report the application of single molecule-based sequencing technology for high-throughput mapping of CFP1, RNA polymerase II and H3K4me3 in mouse brain. By obtaining sequence from chromatin immunoprecipitated DNA, we generated genome-wide binding / chromatin-state maps for mouse brain. We find a good correlation between CFP1 binding and H3K4me3 consistent with it presence in the SetD1 histone methylatransferase complex. Mapped RNA polymerase II colocalised with the majority of CFP1 / H3K4me3 positive CpG islands but not all. This study provides a comprehensive characterisation of the genome wide distribution of a previously uncharacaterised DNA binding factor and suggests a link between DNA base composition and chromatin state. Examination of H3K4me3, RNA PolymeraseII and CFP1 in mouse brain.
2010-04-15 | E-GEOD-18578 | biostudies-arrayexpress
Project description:Spermatogenesis is a complex process involving meiosis in spermatocytes and dynamic epigenetic changes that ensure the inheritance of genetic traits. CXXC finger protein 1 (Cfp1), a component of the SETD1 methyltransferase complex, has a binding domain specific for unmethylated CpG sites. Previous studies have implicated Cfp1 in the epigenetic changes required for meiosis in spermatocytes, and its loss of function has been shown to result in male sterility. In this study, we aimed to gain a comprehensive understanding of Cfp1 function in spermatocytes by examining its genome-wide binding profile and the resulting changes in DNA methylation and H3K4me3, a histone modification associated with active gene transcription. We isolated Cfp1-depleted spermatocytes and performed H3K4me3 ChIP-seq and reduced-representation bisulfite sequencing (RRBS) analyses. By integrating these multi-omics datasets with Cfp1 ChIP-seq analysis, we identified genes directly regulated by Cfp1 and characterised the epigenetic changes associated with its regulation. Our analysis shows that Cfp1 not only directly affects the regulation of genes essential for meiosis, but also has a significant impact on the overall regulation of gene expression. The knowledge gained from studying the regulatory mechanisms of Cfp1 in spermatocytes provides valuable information about the reproductive process and contributes to our understanding of the underlying causes of infertility.
2023-08-10 | GSE240280 | GEO
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is a mark of active and poised promoters. The Set1 complex is responsible for most somatic H3K4me3 and contains the conserved subunit Cfp1, which binds to unmethylated CpGs and links H3K4me3 with CpG islands (CGIs). Here we report that Cfp1 plays unanticipated roles in organising genome wide H3K4me3 in embryonic stem cells. Cfp1-deficiency caused two contrasting phenotypes: drastic loss of H3K4me3 at expressed CGI-associated genes, with minimal consequences for transcription, and creation of ectopic H3K4me3 peaks at numerous regulatory regions. DNA binding by Cfp1 was dispensable for targeting H3K4me3 to active genes, but was required to prevent ectopic H3K4me3 peaks. We analysed gene expression in wild-type, Cfp1-/-, Cfp1wt rescue and Cfp1C169A rescue ES cells on the MouseWG-6 v2.0 Expression BeadChip (Illumina). We found that the presence of ectopic peaks at enhancers often coincided with increased expression of nearby genes. This suggests that CpG targeting prevents leakage of H3K4me3 to inappropriate chromatin compartments. Our results demonstrate that Cfp1 is a specificity factor that integrates multiple signals, including promoter CpG content and gene activity, to regulate genome-wide patterns of H3K4me3.
2012-07-04 | E-MTAB-1198 | biostudies-arrayexpress
Project description:The dinucleotide sequence 5'CG acts as a signalling module that can influence the epigenome and modulate chromosome function. CG exists in three chemically distinct forms that differ due to the modification status of the cytosine base: unmethylated, methylated or hydroxymethylated. The Cfp1 protein binds to unmethylated CG clusters in vivo and is required for the coincident trimethylation of lysine 4 in histone H3 by the Setd1 complex. On the other hand, the methyl-CG binding protein MeCP2 can direct deacetylation of histones. These findings align with evidence that nonmethylated CpG islands mark promoters, whereas CG methylation leads to gene silencing. Interfering with Cfp1 or Mecp2 function will therefore impact chromatin structure, possibly resulting in alteration of transcription. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ Abstract: This project aims to assess effects of Cfp1- and Mecp2-deficiency on transcription using RNA-seq of nascent RNA. This involves in vitro run-on transcription with isolated nuclei using BrU as a substrate to permit purification of nascent RNA. This technique shows where active polymerases are loaded on chromatin, unlike conventional RNA-seq, which only detects stable cytoplasmic RNAs.
2012-06-21 | E-ERAD-80 | biostudies-arrayexpress
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) accumulates at promoters in a gene activity dependant manner. The Set1 complex is responsible for most H3K4me3 in somatic cells and contains the conserved subunit Cfp1, which is implicated in targeting the Set1 complex to CpG islands in mammals. In mouse embryonic stem cells, Cfp1 is necessary for H3K4me3 accumulation at constitutively active gene promoters, but is not required to maintain steady-state transcription of the associated gene. Here we show that Cfp1 is instrumental for targeting H3K4me3 at promoters upon rapid transcriptional induction in response to external stimuli. Surprisingly, H3K4me3 accumulation is not required to ensure appropriate transcriptional output but rather plays gene specific roles. We also show that Cfp1 dependant H3K4me3 deposition contributes to H3K9 acetylation genome wide; suggesting that Cfp1 dependant H3K4me3 regulates overall H3K9 acetylation dynamics and is necessary for histone acetyl transferase recruitment. Finally, we observe increased antisense transcription at start and end of genes that requires Cfp1 for accurate H3K4me3 and H3K9ac deposition. Our results assign a key role for Cfp1 in establishing a complex active promoter chromatin state and shed light on how chromatin signalling pathways provide context dependant outcomes. wt (wtES) or Cfp1-/- (Cfp1null) ES cells were treated or not with doxorubicin (Dox) at 1uM for 6h. H3K4me3 (2 replicates) and H3K9,K14ac (H3ac, 1 replicate) occupancy was analyzed in each condition by ChIP-Seq. Input DNA for each cell line was alos sequenced alongside.
2014-08-20 | E-GEOD-53490 | biostudies-arrayexpress
Project description:Chromatin modifications and the promoter associated epigenome are thought to be important for the regulation of gene expression. However, the mechanisms by which chromatin modifying complexes are targeted to the appropriate gene promoters in vertebrates and how they influence gene expression have remained poorly defined. Here, using a combination of live cell imaging and functional genomics, we discover that the vertebrate SET1 complex is targeted to actively transcribed target gene promoters through CFP1 which engages in a unique form of multivalent chromatin reading that involves recognition of non-methylated DNA and histone H3 lysine 4 trimethylation (H3K4me3). CFP1 defines SET1 complex occupancy on chromatin and its multivalent interactions are required for the SET1 complex to place H3K4me3. In the absence of CFP1, gene expression is perturbed suggesting that the normal targeting and function of SET1 complex is central to creating an appropriately functioning vertebrate promoter associated epigenome.
2017-09-05 | GSE93536 | GEO
Project description:CXXC finger protein 1 (Cfp1) is a DNA-binding component of the SETD1 methyltransferase complex, targets SETD1A/B to most CpG islands (CpGI), and mediates the generation of H3K4me3. Deficiency of CFP1 in mice leads to pre-implantation lethality. Previous data suggest an indispensable role of CFP1 in germ cell development and meiosis. However, it remains unclear if CFP1-mediated H3K4 trimethylation is also required for the earliest stages of meiosis in both male and female germ cells. Here, we revealed that Cxxc1 deletion caused a decrease of H3K4me3 levels in spermatocytes after the zygotene stage, impaired double strand breaks (DSBs) repairing, and crossover formation in meiotic prophase. As the results, Cxxc1-deleted spermatocytes failed to complete meiosis and were arrested at the meiosis II. ChIP-seq results revealed that H3K4me3 globally descreased at transcriptional start sites in Cxxc1-null spermatocytes at the leptotene/zygotene and pathytene stages.RNA-seq at different stages revealed an earlier expression of genes within the spermatogenesis pathway in Cxxc1-null spermatocytes. These results indicated that CFP1 is required for H3K4me3 accumulation at the gene promoters of male germ cells and play a key role in regulating programed gene expression that is essential for spermatogenesis.
2020-03-11 | GSE133636 | GEO
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) accumulates at promoters in a gene activity dependant manner. The Set1 complex is responsible for most H3K4me3 in somatic cells and contains the conserved subunit Cfp1, which is implicated in targeting the Set1 complex to CpG islands in mammals. In mouse embryonic stem cells, Cfp1 is necessary for H3K4me3 accumulation at constitutively active gene promoters, but is not required to maintain steady-state transcription of the associated gene. Here we show that Cfp1 is instrumental for targeting H3K4me3 at promoters upon rapid transcriptional induction in response to external stimuli. Surprisingly, H3K4me3 accumulation is not required to ensure appropriate transcriptional output but rather plays gene specific roles. We also show that Cfp1 dependant H3K4me3 deposition contributes to H3K9 acetylation genome wide; suggesting that Cfp1 dependant H3K4me3 regulates overall H3K9 acetylation dynamics and is necessary for histone acetyl transferase recruitment. Finally, we observe increased antisense transcription at start and end of genes that requires Cfp1 for accurate H3K4me3 and H3K9ac deposition. Our results assign a key role for Cfp1 in establishing a complex active promoter chromatin state and shed light on how chromatin signalling pathways provide context dependant outcomes. wt (wtES) or Cfp1-/- (Cfp1null) ES cells were treated or not with doxorubicin (Dox) at 1uM for 6h and rRNA depleted total RNA was prepraed and analyzed by strand-specific RNA-Seq in 2 biological and 2 technical replicates per condition.
2014-08-20 | E-GEOD-53489 | biostudies-arrayexpress
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) accumulates at promoters in a gene activity dependant manner. The Set1 complex is responsible for most H3K4me3 in somatic cells and contains the conserved subunit Cfp1, which is implicated in targeting the Set1 complex to CpG islands in mammals. In mouse embryonic stem cells, Cfp1 is necessary for H3K4me3 accumulation at constitutively active gene promoters, but is not required to maintain steady-state transcription of the associated gene. Here we show that Cfp1 is instrumental for targeting H3K4me3 at promoters upon rapid transcriptional induction in response to external stimuli. Surprisingly, H3K4me3 accumulation is not required to ensure appropriate transcriptional output but rather plays gene specific roles. We also show that Cfp1 dependant H3K4me3 deposition contributes to H3K9 acetylation genome wide; suggesting that Cfp1 dependant H3K4me3 regulates overall H3K9 acetylation dynamics and is necessary for histone acetyl transferase recruitment. Finally, we observe increased antisense transcription at start and end of genes that requires Cfp1 for accurate H3K4me3 and H3K9ac deposition. Our results assign a key role for Cfp1 in establishing a complex active promoter chromatin state and shed light on how chromatin signalling pathways provide context dependant outcomes.
2014-08-20 | GSE53490 | GEO
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) accumulates at promoters in a gene activity dependant manner. The Set1 complex is responsible for most H3K4me3 in somatic cells and contains the conserved subunit Cfp1, which is implicated in targeting the Set1 complex to CpG islands in mammals. In mouse embryonic stem cells, Cfp1 is necessary for H3K4me3 accumulation at constitutively active gene promoters, but is not required to maintain steady-state transcription of the associated gene. Here we show that Cfp1 is instrumental for targeting H3K4me3 at promoters upon rapid transcriptional induction in response to external stimuli. Surprisingly, H3K4me3 accumulation is not required to ensure appropriate transcriptional output but rather plays gene specific roles. We also show that Cfp1 dependant H3K4me3 deposition contributes to H3K9 acetylation genome wide; suggesting that Cfp1 dependant H3K4me3 regulates overall H3K9 acetylation dynamics and is necessary for histone acetyl transferase recruitment. Finally, we observe increased antisense transcription at start and end of genes that requires Cfp1 for accurate H3K4me3 and H3K9ac deposition. Our results assign a key role for Cfp1 in establishing a complex active promoter chromatin state and shed light on how chromatin signalling pathways provide context dependant outcomes.
2014-08-20 | GSE53489 | GEO