Deignan
Ontology highlight
ABSTRACT:
INSTRUMENT(S): AB SOLiD 4 System
ORGANISM(S): Drosophila melanogaster
SUBMITTER: Leo Zeef
PROVIDER: E-MTAB-1976 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Mutations in the transcription factor p63 underlie of a series of human malformation syndromes which are defined by a combination of epidermal, limb and craniofacial abnormalities including cleft lip and palate. Transcription profiling was performed to determine the role of p63 in vivo mouse palatal shelves. RNA-seq analysis was done of palatal shelves dissected from E10.5, E11.5, E12.5, E13.5 and E14.5 mouse embryos.
2017-06-12 | E-MTAB-3157 | biostudies-arrayexpress
Project description:The SWI/SNF ATP-dependent chromatin remodeler is a master regulator of the epigenome; controlling pluripotency, cell fate determination and differentiation. There is a sparsity of information on the autoregulation of SWI/SNF, the domains involved and their mode of action. We find a DNA or RNA binding module conserved from yeast to humans located in the C-terminus of the catalytic subunit of SWI/SNF called the AT-hook that positively regulates the chromatin remodeling activity of yeast and mouse SWI/SNF. The AT-hook in yeast SWI/SNF interacts with the SnAC and ATPase domains, which after binding to nucleosome switches to contacting the N-terminus of histone H3. Deletion of the AT-hooks in yeast SWI/SNF and mouse esBAF complexes reduces the remodeling activity of SWI/SNF without affecting complex integrity or its recruitment to nucleosomes. In addition, deletion of the AT-hook impairs the ATPase and nucleosome mobilizing activities of yeast SWI/SNF without disrupting the interactions of the ATPase domain with nucleosomal DNA. The AT-hook is also important in vivo for SWI/SNF-dependent response to amino acid starvation in yeast and for cell lineage priming in mouse embryonic stem cells. In summary, the AT-hook is shown to be an evolutionarily conserved autoregulatory domain of SWI/SNF that positively regulates SWI/SNF both in vitro and in vivo.
2023-06-15 | PXD040664 | Pride
Project description:ChIP-seq profiles for CTCF and TGF-beta signaling factors before and after treatment with DPP Examination of transcription factor dynamics during signaling
2015-05-08 | E-GEOD-68654 | biostudies-arrayexpress
Project description:Histone H3 lysine27-to-methionine (H3K27M) gain-of-function mutations occur in highly aggressive pediatric gliomas. Here, we establish a Drosophila animal model for the pathogenic histone H3K27M mutation and show that its overexpression resembles Polycomb repressive complex 2 (PRC2) loss-of-function phenotypes, causing de-repression of PRC2 target genes and developmental perturbations. Similarly, a H3K9M mutant depletes H3K9 methylation levels and suppresses position-effect variegation in various Drosophila tissues. The histone H3K9 demethylase KDM3B/JHDM2 associates with H3K9M nucleosomes and its overexpression in Drosophila results in loss of H3K9 methylation levels and heterochromatic silencing defects. Here we establish histone lysine-to-methionine mutants as robust in vivo tools for inhibiting methylation pathways that also function as biochemical reagents for capturing site-specific histone-modifying enzymes, thus providing molecular insight into chromatin-signaling pathways. RNA-seq of wing imaginal discs expressing either H3.3WT-FLAG-HA or H3.3K27M-FLAG-HA.
2014-09-02 | E-GEOD-59891 | biostudies-arrayexpress
Project description:The molecular mechanisms regulating tissue size represent an unsolved puzzle in developmental biology. One signaling pathway controlling growth of the Drosophila wing is Dpp. Dpp promotes growth via repression of the transcription factor Brinker. The transcriptional targets of Brinker that control cell growth and proliferation, however, are not yet fully elucidated. We report here a genome-wide ChIP-seq of endogenous Brinker from wing imaginal discs. We identify the growth regulator Myc as a target of Brinker and show that Myc together with the microRNA bantam explain a large fraction of the growth inhibition caused by Brinker. This work sheds light on the effector mechanisms by which Dpp signaling controls tissue growth. Identification of Brinker binding sites in Wing imaginal discs cells
2013-01-29 | E-GEOD-40957 | biostudies-arrayexpress
Project description:Like many microalgae unicellular green alga, Chlamydomonas reinhardtii also accumulates energy rich storage lipid and starch under nutrient-limited conditions, such as phosphorus (P) and nitrogen (N) limitation. To dissect the transcriptional regulation of lipid and starch biosynthesis in response to nutrient limitation, we have characterized the biological role of a candidate regulator: the MYB family transcription factor, PSR1 (phosphorus starvation response 1). Genetically modified (psr1 compromised) and wild-type lines were grown under P limiting and sufficient conditions and assayed at two time points by SOLiD RNA-seq.
2016-01-08 | E-MTAB-2556 | biostudies-arrayexpress
Project description:Piwi proteins and their associated small RNAs are essential for fertility in animals. This is due, in part, to their roles in guarding germ cell genomes against the activity of mobile genetic elements. piRNA populations direct Piwi proteins to silence transposon targets and as such form a molecular code that discriminates transposons from endogenous genes. Information ultimately carried by piRNAs is encoded within genomic loci, termed piRNA clusters. These give rise to long, single-stranded, primary transcripts that are processed into piRNAs. Despite the biological importance of this pathway, neither the characteristics that define a locus as a source of piRNAs nor the mechanisms that catalyze primary piRNA biogenesis are well understood. We searched an EMS-mutant collection annotated for fertility phenotypes for genes involved in the piRNA pathway. Twenty-seven homozygous-sterile strains showed transposon-silencing defects. One of these, which strongly impacted primary piRNA biogenesis, harbored a causal mutation in CG5508, a member of the Drosophila glycerol-3-phosphate O-acetyltransferase (GPAT) family. These enzymes catalyze the first acylation step on the path to the production of phosphatidic acid (PA). Though this pointed strongly to a function for phospholipid signaling in the piRNA pathway, a mutant form of CG5508, which lacks the GPAT active site, still functions in piRNA biogenesis. We have named this new biogenesis factor Minotaur. Examination of transcriptom profile in heterozygous and homozygous CG5508 mutant ovaries
2013-04-27 | E-GEOD-46423 | biostudies-arrayexpress
Project description:We performed H3K9me2-based ChIP-seq to identify regions of the Drosophila genome that are H3K9me2-depleted due to transgenic neuronal expression of human mutant tau. Examination of H3K9me2 histone methylation in 10 day old control and tau transgenic Drosophila heads.
2013-12-31 | E-GEOD-53719 | biostudies-arrayexpress
Project description:Mutants of the Mnn1 gene are hyper-sensitive to several stresses and display increased genome instability when subjected to conditions, such as heat shock, generally regarded as non-genotoxic. We describe a role for Menin as a global regulator of heat shock gene expression and critical factor in the maintenance of genome integrity 2-colour microarray design using 36 microarrays testing shock vs non shock in Drosophila melanogaster. Using a test of loss-of-heterozygosity, we show that Drosophila strains lacking a functional Mnn1 gene or expressing a Mnn1 dsRNAi are characterized by increased genome instability in response to short, repeated but non-lethal heat shock or hypoxia treatments. The same was true for strains lacking all Hsp70 genes.
2010-10-25 | E-GEOD-20497 | biostudies-arrayexpress
Project description:We describe the epigenetic profiling of the H3K9me2 and HP1a in Drosophila third instar larvae before and after CDK12 depletion by RNA interference (RNAi). Here we show that CDK12 regulates heterochromatin dynamics in Drosophila chromosomes. Depletion of CDK12 induces the increased HP1a and H3K9me2 binding profile on the coding region of euchromatic genes, with the X chromosome being the most affected. These results are consistent with the polytene chromosome immunostaining pattern of HP1a and H3K9me2 after CDK12 knockdown in our initial cytological observations, which show that CDK12 depletion induce heterochromatin spreading on euchromatic arms, especially on the X chromosome. This study describes a novel role of the CDK12 complex in controlling the epigenetic transition between euchromatin and heterochromatin. Examination of the genome-wide H3K9me2 and HP1a binding profile in wildtype larvae (WT) and CDK12-depleted larvae (CDK12-KD). Examination of the genome-wide CDK12 binding profile in wildtype larvae (WT). Twelve independent immunoprecipitations were conducted for each antibody. Two biological replicates were performed.
2015-11-02 | E-GEOD-63011 | biostudies-arrayexpress