Transcriptomic regulation and methylation of the Lysine4 of Histone H3 during meiosis
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE11004 | GEO | 2008/11/01
SECONDARY ACCESSION(S): PRJNA107085
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE10836: Meiotic time course of Histone H3 occupancy GSE10837: Meiotic time course of the trimethylation of the Lysine 4 of Histone H3 (H3K4me3) in a mutant Spo11F GSE10838: Meiotic time course of Histone H3 occupancy in a mutant Spo11F GSE10839: Meiotic time course of the trimethylation of the Lysine 4 of Histone H3 (H3K4me3) in a mutant clb5Delta-clb6Delta GSE10840: Meiotic time course of the trimethylation of the Lysine 4 of Histone H3 (H3K4me3) GSE10944: Transcriptomic regulation during meiosis GSE10947: Transcriptomic regulation during meiosis (Spo11Y135F mutant) GSE10948: Transcriptomic regulation during meiosis (Clb5Delta-Clb6Delta mutant) GSE12879: Meiotic DNA double strand breaks in wild-type and set1 cells Keywords: SuperSeries Refer to individual Series
2008-10-31 | E-GEOD-11004 | biostudies-arrayexpress
Project description:Transcriptomic regulation and methylation of the Lysine4 of Histone H3 during meiosis
| PRJNA107085 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-02-10 | E-GEOD-75169 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-02-10 | GSE75169 | GEO
Project description:The molecular signature at histone H3K4me3 and H3K27me3 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3, associated with active chromatin, and H3K27me3, associated with repressed chromatin, histone modifications to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes.
2016-03-24 | GSE77772 | GEO
Project description:The molecular signature at histone H3K4me3 and H3K27me3 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3, associated with active chromatin, and H3K27me3, associated with repressed chromatin, histone modifications to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. histone H3K4me3 and H3K27me3 ChIP-seq normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells Please note that the 'H3K4me3' and 'input' data are duplicated records of the samples represented in GSE69377 for the convenient retrieval of the complete raw data from SRA.
2016-03-24 | E-GEOD-77772 | biostudies-arrayexpress
Project description:Menin, encoded by the multiple endocrine neoplasia type 1 (MEN1) gene, is a tumor suppressor that leads to multiple endocrine tumors upon loss of its function. Menin functions as a transcriptional activator by tethering MLL complex to mediate histone H3 K4 methylation. It also functions as a repressor. However, the molecular mechanism of how menin contributes to the opposite outcome in gene expression is largely unknown. Here, we investigated the role of menin in the epigenetic regulation of transcription mediated by histone covalent modification. We show that the global methylation level of histone H3 K9, as well as H3 K4, was decreased in Men1(-/-) MEF cells. Consistently, menin was able to interact with the suppressor of variegation 3-9 homolog family protein, SUV39H1, to mediate H3 K9 methylation. This interaction decreased when patient-derived MEN1 mutation was introduced into the SUV39H1-interaction domain. We show that menin mediated different chromatin changes depending on target genes. Chromatin immunoprecipitation studies showed that menin directly associated with the GBX2 promoter and menin-dependent recruitment of SUV39H1 was essential for chromatin remodeling and transcriptional regulation. These results provide a molecular basis of how menin functions as a transcriptional repressor and suggest that menin-dependent integration of H3 K9 methylation might play an important role in preventing tumors.
| S-EPMC3668625 | biostudies-literature
Project description:Histone post-translational modifications are key contributors to chromatin structure and function, and participate in the maintenance of genome stability. Understanding the establishment and maintenance of these marks, along with their misregulation in pathologies is thus a major focus in the field. While we have learned a great deal about the enzymes regulating histone modifications on nucleosomal histones, much less is known about the mechanisms establishing modifications on soluble newly synthesized histones. This includes methylation of lysine 9 on histone H3 (H3K9), a mark that primes the formation of heterochromatin, a critical chromatin landmark for genome stability. Here, we report that H3K9 mono- and dimethylation is imposed during translation by the methyltransferase SetDB1. We discuss the importance of these results in the context of heterochromatin establishment and maintenance and new therapeutic opportunities in pathologies where heterochromatin is perturbed.
| S-EPMC4627087 | biostudies-literature
Project description:The hippocampal formation is a brain region noted for its plasticity in response to stressful events and adrenal steroid hormones. Recent work has shown that chromatin remodeling in various brain regions, including the hippocampus, is associated with the effects of stress in a variety of models. We chose to examine the effects of stress, stress duration, corticosterone administration, and fluoxetine treatment on the levels of hippocampal histone H3 methylation at lysines 4, 9, and 27, marks associated, respectively, with active transcription, heterochromatin formation, and transcriptional repression. We found that acute stress increased the levels of H3K9 tri-methylation (H3K9me3) in the dentate gyrus (DG) and CA1, while it reduced levels of H3K9 mono-methylation (H3K9me1) and H3K27 tri-methylation (H3K27me3) in the same regions, and had no effect on levels of H3K4 tri-methylation (H3K4me3). Seven days of restraint stress reduced levels of H3K4me3 in the CA1 and H3K27me3 in the DG and CA1, while increasing basal levels of H3K9me3. Chronic restraint stress (CRS) for 21 days mildly increased levels of H3K4me3 and reduced H3K9me3 levels in the DG. Treatment with fluoxetine during CRS reversed the decrease in DG H3K9me3, but had no effect on the other marks. These results show a complex, surprisingly rapid, and regionally specific pattern of chromatin remodeling within hippocampus produced by stress and anti-depressant treatment that may open an avenue of understanding the interplay of stress and hippocampal gene expression, and reveal the outlines of a potential chromatin stress response that may be diminished or degraded by chronic stress.
| S-EPMC2791599 | biostudies-literature
Project description:Plants undergo extensive reprogramming of chromatin status during sexual reproduction, a process vital to cell specification and pluri- or totipotency establishment. As a crucial way to regulate chromatin organization and transcriptional activity, histone modification can be reprogrammed during sporogenesis, gametogenesis, and embryogenesis in flowering plants. In this review, we first introduce enzymes required for writing, recognizing, and removing methylation marks on lysine residues in histone H3 tails, and describe their differential expression patterns in reproductive tissues, then we summarize their functions in the reprogramming of H3 lysine methylation and the corresponding chromatin re-organization during sexual reproduction in Arabidopsis, and finally we discuss the molecular significance of histone reprogramming in maintaining the pluri- or totipotency of gametes and the zygote, and in establishing novel cell fates throughout the plant life cycle. Despite rapid achievements in understanding the molecular mechanism and function of the reprogramming of chromatin status in plant development, the research in this area still remains a challenge. Technological breakthroughs in cell-specific epigenomic profiling in the future will ultimately provide a solution for this challenge.
| S-EPMC8669150 | biostudies-literature