Project description:The epidermis is a stratified squamous epithelium that serves to protect the body from dehydration, absorption of chemicals, and invasion of pathogens. In the epidermis, cells of the basal layer contain proliferative potential. As they divide and move upward in the tissue, they progressively differentiate, and activate the gene expression program required to create a barrier; eventually, cells in the uppermost layer are sloughed off from the surface of the epidermis. This system requires continual replacement of differentiating cells from the basal layer. Such a process requires very precise regulation of gene expression to balance proliferation and differentiation and maintain a functioning epithelium. Epigenetic mechanisms of gene regulation, including DNA methylation and histone modification have been shown to play a major role in tissue development and wound healing. To identify regulatory regions in differentiating epidermal cells, we performed ChIP-Seq with antibodies to H3K4me1, and H3K4me3 at 24 hours after induction of differentiation to complement publicly available ENCODE data for these marks in undifferentiated NHEK. With this data, we were able to identify enhancers, defined by the presence of high levels of H3K4me1 and H3K27ac, and low levels of H3K4me3. We identified approximately 20,000 of these regions each in undifferentiated and differentiated keratinocytes. Approximately 20 percent of these regions were shared between the two conditions, while about 30 and 43 percent were unique to differentiated and undifferentiated keratinocytes, respectively.
Project description:We report the impact of the pharmacological inhibition of the Histone 3 Lysine 4 demethylase (H3K4) LSD1 (KDM1A) enzymatic activity on its binding genome wide and how it impacts genome-wide H3K4me1 and H3K4me2 deposition in Normal Human Epidermal Keratinocytes (NHEK)
Project description:In this study we have examine the deposition of H3K4me1,H3K4Me3 and H3K27Ac and the Nodal transcription factor, Smad2/3, immediately following zygotic transcription and continuing through gastrulation. We profiled 4 histone modifications (H3K4Me3, H3K27Me3, H3K27AC, H3K4Me1) and one transcription factor smad2/3 (+ chromatin input) using ChIP-Seq, and expression profiles (3' RNA-Seq) for Xenopus tropicalis embryos stage8, stage9 and stage10.5. Furthermore, we have profile two histone modifications (H3K4Me1 and H3K27Ac) in absance of nodal signaling in stage9 Xenopus tropicalis embryos using ChIP-seq and 3-seq
Project description:ChIP-seq data (H3K4Me1, H3K4Me3, H3K27Ac histone modifications) on multiple myeloma cell line KMS11 and plasma cell leukaemia cell lines L363 and JJN3
Project description:<p>The primary goal of this study was to collect and analyze genomic data from primary glioblastoma multiforme tumors. Our collaborators at St David's Medical Center (SDMC) obtained informed consent from patients undergoing surgery to remove a tumor in the brain. After consent was obtained, specimens were removed from the operating suite and flash frozen in liquid nitrogen. Tumors were analyzed if they were a grade III (anaplastic astrocytoma) or grade IV glioma (glioblastoma multiforme). Tumors were transported from SDMC to UT Austin, then weighed and homogenized. Chromatin immunoprecipitation was performed for 7 proteins in each tumor (histone modifications H3K4me3, H3K4me1, H3K9ac, H3K9me3, H3K27ac, H3K27me3, and the multifunctional insulator binding protein CTCF) and no-antibody input was also sequenced. An aliquot of tumor material was set aside for isolation of total RNA.</p>
Project description:Here we present the whole genome ChIP-Seq analyses of a wide variety of histone marks, H3K27ac, H3K4me1, H3K4me3, and H3K27me3 in the brain, heart, and liver, along with the RNA-seq data of these organs of early human embryos 12 weeks after gestation. In total, brain, heart, and liver of early human post-implantation embryos were used, and four histone modifications were detected, including H3K27ac, H3K4me1, H3K4me3 and H3K27me3. Also, the transcriptomes of these three organs were analyzed.
Project description:We did ChIP-seq with anti- H3K4me3, H3K4me1, H3K4me2, H3K27me3, H3K27ac, and H3K36me3 antibodies in both C2C12 myoblasts and myotubes Examination of 6 different histone modifications in 2 cell types.
Project description:Analysis of keratinocyte differentiation in presence or absence of fibroblast-derived JNK-dependent soluble factors in vitro. The hypothesis tested in the present study was that JNK-dependent fibroblast-derived soluble factors promote an efficient keratinocyte differentiation. Results provide important information about reduced expression of a subset of differentiation associated genes in keratinocytes in the absence of JNK-dependent fibroblast-derived soluble factors. In vitro transwell co-culture experiments were performed using jnk1-/-jnk2-/- or wildtype immortalized mouse embryonic fibroblasts (MEFs) and differentiating primary normal human epidermal keratinocytes (NHEK) over a time course of 6 days. Total RNA was obtained from NHEK prior to cultivation with MEFs (day 0) and every second day (days 2, 4, and 6) during co-culture. MEFs have been described previously in Sabapathy et al. (2004) Mol Cell 15:713-25.
Project description:Considered as fundamental epigenetic regulators controlling many key cellular processes, histone modifications are a well-conserved and widely studied class of epigenetic modifications. Genome-wide studies have identified enhancers as DNA sequences that bind to H3K4me1 and H3K27ac and promoters as DNA sequences that bind to H3K4me3. To explore how the Twist1 complex (Twist1/YY1/p300) regulates miR-9 expression, we performed ChIP-seq in PLC-PRF-5 cells, providing a panorama of p300, H3K4me3, H3K4me1, and H3K27ac.
Project description:We generated genome-wide chromatin state and RNA Polymerase II binding maps in mouse erythroid cells by ChIP-Seq. Examination of 4 different histone modifications (H3K4me3, H3K4me1, H3K27me3, H3K27ac) and RNA Polymerase II (RNAP2) binding in mouse erythroid cells (Ter119+).
