Daily cycling of genome-wide histone methylation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Utham Valekunja
PROVIDER: E-GEOD-37393 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-01-01 | E-GEOD-37396 | biostudies-arrayexpress
Project description:Daily (circadian) clocks are essential for regulating and coordinating physiology in mammals. Modulation of local chromatin structure has been shown for only a small number of genes, principally thought to be directly modulated by Clock-mediated histone acetylation. Here we show that genome-wide changes of active and suppressive histone marks control global chromatin architecture over the day and night. Examination of mouse liver tissue at 4 time-points around the clock in "free-running", continuous conditions (constant darkness, temperature and food available ad libitum).
2013-01-08 | E-GEOD-23550 | biostudies-arrayexpress
Project description:Peripheral circadian clocks regulate many aspects of physiology. In this study we deleted the core circadian clock component Bmal1 specifically in mouse adipocytes in order to study the role of the adipocyte clock in energy homeostasis and body weight. We used microarrays to indentify changes in gene expression in the adipose tissue of mice lacking a functional adipocyte circadian clock and identified a small number of up- and down- regulated genes. Adipose tissues were isolated from inguinal adipose fat pads at four different times of the diurnal cycle under constant darkness (circadian time, CT) for RNA extraction and hybridization on Affymetrix microarrays. Adipocyte-specific Bmal1 KO (Ad-Bmal1-/-) and control mice were used for isolation of tissues at CT0, CT6, CT12, CT18 where CT0 the beginning of the subjective day.
2012-10-21 | E-GEOD-35026 | biostudies-arrayexpress
Project description:Under continuous, glucose-limited conditions, budding yeast exhibit robust metabolic cycles associated with major oscillations of gene expression and metabolic state. However, how such fluctuations might be coordinately linked to changes in chromatin status is less well understood. Here, we examine the correlated genome-wide transcription and chromatin states across the yeast metabolic cycle (YMC) at unprecedented temporal resolution, revealing a "just in time supply chain" by which specific cellular processes such as ribosome biogenesis are coordinated in time with remarkable precision. We identify distinct chromatin and splicing patterns associated with different gene categories and determine the relative timing of chromatin modifications to maximal transcription. Additionally, we interrogate chromatin modifier occupancy and observe subtly distinct spatial and temporal patterns compared to the modifications themselves. Furthermore, we identify multiple lysine mutants in H3 or H4 tails that disrupt metabolic cycling, supporting a potentially cooperative role of histone modifications in the YMC. 16 time points RNA-seq and ChIP-seq of 8 histone marks over one metabolic cycle, 14 time points ChIP-seq of 3 chromatin modifiers over one metabolic cycle
2014-08-31 | E-GEOD-52339 | biostudies-arrayexpress
Project description:DNA methylation at the 5-position of cytosine (5-mC) is a key epigenetic mark critical for varius biological and pathological processes. 5-mC can be converted to 5-hydroxymethylcytosine (5-hmC) by the Ten-Eleven Translocation (TET) family of DNA hydroxylases. Here we report that "loss of 5-hmC" is an epigenetic hallmark of melanoma with diagonostic and prognostic implications. Genome-wide mapping of 5-hmC in nevi and melanomas for the first time revealed loss of 5-hmC landscape in the melanoma epigenome. Downregulation of Isocitrate Dehydrogenase 2 (IDH2) and TET family enzymes proved to be one of the mechanisms underlying the loss of 5-hmC during melanoma development, and rebuilding the 5-hmC landscape in the melanoma epigenome by reintroducing active TET2 or IDH2 suppressed melanoma growth and increased tumor-free survival. Thus, our study establishes that "loss of 5-hmC" is a new epigenetic hallmark of melanoma and links IDH and TET family enzymes-mediated 5-hmC putative tumor suppressor pathway to the suppression of melanoma progression. Determine the genome-wide distribution of 5mC and 5hmC in benign nevus tissue, melanoma tissue, A2058 MOCK cells (overexpressing empty vector), A2058 TET2 cells (overexpressing wild type human TET), and A2058 TET2M cells (overexpressing mutant human TET).
2012-09-18 | E-GEOD-38231 | biostudies-arrayexpress
Project description:The evolutionarily conserved cohesin complex is crucial for holding sister chromatids together from the time of DNA replication until their segregation during the metaphase to anaphase transition. Human diseases associated with with mutations in the cohesin network are termed "cohesinopathies". Scc2 is required for loading cohesin onto DNA prior to DNA replication. Cornelia de Lange syndrome (CdLS), a developmental disorder characterized by growth and intellectual impairment is caused by mutations in Scc2. How mutations in Scc2 gives rise to these developmental defects is currently unknown, as overt defects in chromosome segregation are not observed in CdLS patients. One hypothesis is that, reduced binding of Scc2 causes gene misregulation. To further explore this idea ChIP-seq was performed using an scc2-4 mutant. We observed from the analysis, we observe reduce binding of Scc2 to Pol II transcribed genes (snoRNAs, ribosomal protein genes) and pol II transcribed genes (tRNAs). Studies are currently underway to examine the biological implications of this observation. Examining genome-wide binding of scc2-4 mutant
2015-06-16 | E-GEOD-55357 | biostudies-arrayexpress
Project description:The mammalian circadian clock is a molecular oscillator composed of a feedback loop that involves transcriptional activators CLOCK and BMAL1, and repressors Cryptochrome (CRY) and Period (PER). Here we show that a direct CLOCK-BMAL1 target gene, Gm129, is a novel regulator of the feedback loop. ChIP analysis revealed that the CLOCK:BMAL1:CRY1 complex strongly occupies the promoter region of Gm129. Both mRNA and protein levels of GM129 exhibit high amplitude circadian oscillations in mouse liver, and Gm129 gene encodes a nuclear-localized protein that directly interacts with BMAL1 and represses CLOCK:BMAL1 activity. In vitro and in vivo protein-DNA interaction results demonstrate that, like CRY1, GM129 functions as a repressor by binding to the CLOCK:BMAL1 complex on DNA. Although Gm129-/- or Cry1-/- Gm129-/- mice retain a robust circadian rhythm, the peaks of Nr1d1 and Dbp mRNAs in liver exhibit significant phase delay compared to control. Our results suggest that, in addition to CRYs and PERs, GM129 protein contributes to the transcriptional feedback loop by modulating CLOCK:BMAL1 activity as a transcriptional repressor. Examination of 3 transcriptional regulators in mouse liver
2014-01-07 | E-GEOD-53828 | biostudies-arrayexpress
Project description:To systematically understand how the circadian clock and the nutrient-driven rhythm integrate to regulate SREBP1 activity, we evaluated genome-wide the binding of SREBP1 to its targets along the day in wild-type (WT) C57BL/6mice. The recruitment of SREBP1 to the DNA showed a highly circadian behaviour, with a maximum during the fed status. However, the temporal expression of SREBP1 targets was not always synchronized with its binding. In particular, a different phase of expression was observed for SREBP1 target genes depending on their function, suggesting the involvement of other transcription factors in their regulation. The proper temporal expression pattern of these genes was dramatically changed in Bmal1KO mice upon time-restricted feeding, in spite of the rhythmic, although slightly delayed, binding of SREBP1. Our results show that besides the nutrient-driven regulation of SREBP1 nuclear translocation, a second layer of modulation of SREBP1 transcriptional activity exists and is strongly dependent from the circadian core clock. This system allows to fine tune the expression timing of SREBP1 target genes, thus helping to temporally separate the different physiological processes in which these genes are involved. 6 samples examined, 6 SREBP1 samples, as well as 6 Polr2b and 6 input samples from GEO series GSE35788 CycliX Consortium was a contributor to this submission.
2014-03-10 | E-GEOD-48375 | biostudies-arrayexpress
Project description:Circadian clocks have evolved as time-measuring molecular devices to help organisms adapt their physiology to daily changes in light and temperature. Cycling transcription has been long hypothesized to account for the wealth of rhythmic protein abundance. However, cyclic degradation signals such as ubiquitylation could shape the rhythmic protein landscape as well. In order to document the circadian ubiquitylated proteome of Drosophila melanogaster, we took advantage of a new means of Ub purification based on in vivo biotinylation of AviTag-tagged ubiquitin by the BirA protein, the bioUb system. NeutrAvidin-bound fractions of head lysates were collected at four circadian times six hours apart and proteins were identified and quantified using a proteomic-based approach.
2018-05-22 | PXD005015 | Pride
Project description:We show that target mRNAs trigger the non-templated addition of nucleotides (mainly adenosines and uridines) and shortening of their cognate miRNAs in primary hippocampal neurons. The induced effect is observable both in total RNA and in Ago2-associated RNA, demonstrating that the process is initiated in Ago2 bound miRNAs. Illumina Small RNA sequencing was performed on rat hippocampal neurons infected with different target mRNAs in different conditions. The data includes 3 independent experiments: 1. Hippocampal neurons (DIV15) 6 days after transducing them with target mRNAs (driven by the Synapsin promoter) against different miRNAs. Samples are titled "Syn-Target". Samples transduced with targets containing extensive complementarity are labeled "Ext" and those with Seed complementarity are labeled "Seed". 2. Hippocampal neurons (DIV16) 7 days after transducing them with an inducible target mRNA against miR-132, and inducing for different times with Doxycycline. Samples are titled "Time-course" 3. Hippocampal neurons (DIV16) 7 days after co-transducing them with FLAG/HA-Ago2 plus an inducible target mRNA against miR-132, and inducing them for different times with Doxycycline. Samples are titled "Time-course_Ago2"
2015-03-02 | E-GEOD-57663 | biostudies-arrayexpress