Gallus gallus
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ABSTRACT:
PROVIDER: PRJNA152767 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from H2A.Z isoforms single KO cells
| PRJNA301232 | ENA
Project description:The histone variant H2A.Z is evolutionarily conserved from yeast to vertebrates. H2A.Z regulates gene expression when localized to promoter region. Recently, we identified two genes encoding H2A.Z, H2A.Z-1 and H2A.Z-2 in vertebrate genome. However, it is not clear that both H2A.Z-1 and H2A.Z-2 were required for the function of H2A.Z in gene regulation. To address this issue, we generated the H2A.Z-1 and H2A.Z-2 double knock out (KO) cells in chicken DT40 cells. The expression pattern of H2A.Z-1 and H2A.Z-2 double KO cells was compared with WT cells to characterize the genes regulated by H2A.Z-1 and H2A.Z-2. We used microarrays to analysis the alternation of gene expression between WT and H2A.Z double KO cells and identify classes of up or down regulated gene by H2A.Z-1 and H2A.Z-2. In H2A.Z-1 and H2A.Z-2 double KO cells, H2A.Z-2 is knocked out constitutively, but H2A.Z-1 conditionally by tetracycline. The expression of H2A.Z-1 transgene is suppressed completely when H2A.Z-1 and H2A.Z-2 double KO cells culture with tetracycline for three days. For this reason, we prepared the total RNA of WT cells and H2A.Z-1and H2A.Z-2 double KO cells treated with tetracycline for three days and hybridization on Affymetrix microarrays.
2015-11-04 | E-GEOD-35430 | biostudies-arrayexpress
Project description:The histone variant H2A.Z is evolutionarily conserved from yeast to vertebrates. H2A.Z regulates gene expression when localized to promoter region. Recently, we identified two genes encoding H2A.Z, H2A.Z-1 and H2A.Z-2 in vertebrate genome. However, it is not clear that both H2A.Z-1 and H2A.Z-2 were required for the function of H2A.Z in gene regulation. To address this issue, we generated the H2A.Z-1 and H2A.Z-2 double knock out (KO) cells in chicken DT40 cells. The expression pattern of H2A.Z-1 and H2A.Z-2 double KO cells was compared with WT cells to characterize the genes regulated by H2A.Z-1 and H2A.Z-2. We used microarrays to analysis the alternation of gene expression between WT and H2A.Z double KO cells and identify classes of up or down regulated gene by H2A.Z-1 and H2A.Z-2.
2015-11-04 | GSE35430 | GEO
Project description:The histone variant H2A.Z is evolutionarily conserved from yeast to vertebrates. H2A.Z regulates gene expression when localized to promoter region. Recently, we identified two genes encoding H2A.Z, H2A.Z-1 and H2A.Z-2 in vertebrate genome. However, it is not clear that both H2A.Z-1 and H2A.Z-2 were required for the function of H2A.Z in gene regulation. To address this issue, we generated the H2A.Z-1 and H2A.Z-2 single knockout cells in chicken DT40 cells.We used microarrays to analysis the alternation of gene expression profiles in H2A.Z-1 KO and H2A.Z-2 KO cells and identify classes of up or down regulated gene by H2A.Z-1 and H2A.Z-2.
2024-10-19 | GSE74715 | GEO
Project description:A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.
2025-03-01 | GSE262044 | GEO
Project description:To understand how chromatin structure is organized by different histone variants, we have measured the genome-wide distribution of nucleosome core particles (NCPs) containing the histone variants H3.3 and H2A.Z in human cells. We find that a special class of NCPs containing both variants is enriched at ‘nucleosome-free regions’ of active promoters, enhancers and insulator regions. We show that preparative methods used previously in studying nucleosome structure result in the loss of these unstable double-variant NCPs. It seems likely that this instability facilitates the access of transcription factors to promoters and other regulatory sites in vivo. Other combinations of variants have different distributions, consistent with distinct roles for histone variants in the modulation of gene expression. genome-wide analysis of histone variants H2AZ, H3.3, and H3.3-H2A.Z double ChIP, plus input and genomic DNA controls in HeLa cells. H2A.Z samples are prepared under two different salt concentration conditions. (6 samples in total)
2009-07-26 | E-GEOD-13308 | biostudies-arrayexpress
Project description:We report a genome wide enrichment, redistribution and accumulation of H2A.Z at specific chromatin control regions, in particular at enhancers and insulators, in mouse embryonic fibroblasts depleted for Anp32e (MEFs Anp32e-/-). H2A.Z ChIP-seq in MEFs WT (+/+) or KO (-/-) for Anp32e.
2014-01-22 | E-GEOD-51579 | biostudies-arrayexpress
Project description:Expression data from single embryonic chick retinal cells
| PRJNA345503 | ENA
Project description:While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.
2020-04-18 | GSE148865 | GEO
Project description:A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.
2025-03-01 | GSE262049 | GEO