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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide chromatin analysis of wing imaginal discs

ABSTRACT: We report the relationship between 'absent, small or homeotic discs 2' (ASH2) occupancy, histone modifications and the transcription machinery using the wing disc as a source of chromatin. Our results indicate that genes related to development and transcriptional regulation are direct targets of ASH2 and that this protein contributes to H3K4me3 of nearby nucleosomes. Moreover, ASH2 occupancy correlates with phosphorylated forms of RNA polymerase II and histone positive marks in active genes. RNA Pol II phosphorylation in Ser5 is reduced in ash2 mutants, indicating that ASH2 plays a role in promoter stalling. Examination of three histone modifications and two polymerase modifications in wing imaginal dics cells.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Enrique Blanco

PROVIDER: E-GEOD-24115 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide chromatin occupancy analysis reveals a role for ASH2 in transcriptional pausing.

Pérez-Lluch Sílvia S Blanco Enrique E Carbonell Albert A Raha Debasish D Snyder Michael M Serras Florenci F Corominas Montserrat M

Nucleic acids research 20110209 11

An important mechanism for gene regulation involves chromatin changes via histone modification. One such modification is histone H3 lysine 4 trimethylation (H3K4me3), which requires histone methyltranferase complexes (HMT) containing the trithorax-group (trxG) protein ASH2. Mutations in ash2 cause a variety of pattern formation defects in the Drosophila wing. We have identified genome-wide binding of ASH2 in wing imaginal discs using chromatin immunoprecipitation combined with sequencing (ChIP-S ...[more]

PMID: 21310711

Similar Datasets

Genome-wide chromatin analysis of wing imaginal discs

Project description:We report the relationship between 'absent, small or homeotic discs 2' (ASH2) occupancy, histone modifications and the transcription machinery using the wing disc as a source of chromatin. Our results indicate that genes related to development and transcriptional regulation are direct targets of ASH2 and that this protein contributes to H3K4me3 of nearby nucleosomes. Moreover, ASH2 occupancy correlates with phosphorylated forms of RNA polymerase II and histone positive marks in active genes. RNA Pol II phosphorylation in Ser5 is reduced in ash2 mutants, indicating that ASH2 plays a role in promoter stalling.

2011-02-17 | GSE24115 | GEO

A large-scale, in vivo transcription factor screen defines bivalent chromatin as a key property of regulatory factors mediating Drosophila wing development

Project description:ChIP-seq to map enrichment of histone modifications and RNA polymerase II DNA occupancy in imaginal wing discs at 120 h of development.

2014-12-30 | GSE59769 | GEO

Analysis of the trithorax Group (trxG) genes ash2 and ash1 wing imaginal disc transcriptomes.

Project description:The absent, small or homeotic discs 2 (ash2) gene, a member of the trithorax Group (trxG) of transcriptional regulators, is functionally related to ash1. However, ASH2 and ASH1 belong to distinct multimeric complexes of unknown composition and it is unclear how they act to regulate transcription. In this study, examination of gene expression profiles in wing imaginal discs from ash2 and ash1 mutants revealed their transcriptomes are very similar and correlate with wing phenotypes. Keywords: loss of function analysis

2007-07-31 | GSE4923 | GEO

Brinker regulates wing disc growth in part via repression of Myc expression

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

Chromatin immunoprecipitation of yeast to assess changes in RNA Polymerase II, Ser5-P, and Ser7-P occupancy upon chemical inhibition of Kin28

Project description:Chromatin Immunoprecipitation to assess changes in RNA Polymerase II, Ser5-P, and Ser7-P occupancy in S. cerevisiae upon chemical inhibition of Kin28

2009-07-01 | E-TABM-689 | biostudies-arrayexpress

Nuclear myosin 1 contributes to a chromatin landscape compatible with RNA polymerase II transcription activation

Project description:Nuclear myosin 1c (NM1) is emerging as regulator of transcription and chromatin organization. Using a genome-wide approach we report here that NM1 binds across the mammalian genome with occupancy peaks at class II gene promoters, correlating with distributions of RNA Polymerase II (Pol II) and active epigenetic marks. We show that NM1 synergizes with polymerase-associated actin to maintain active Pol II at gene promoters. NM1 also co-localizes with the nucleosome remodeler SNF2h at class II promoters where they assemble together with WSTF as part of the B-WICH complex to remodel chromatin. Following B-WICH assembly, NM1 mediates physical recruitment of the histone acetyl transferase PCAF and the histone methyl transferase Set1/Ash2 to maintain and preserve H3K9acetylation and H3K4trimethylation for active transcription. We propose a novel genome-wide mechanism where myosin synergizes with Pol II-associated actin to link the polymerase machinery with permissive chromatin for transcription activation. Association of nuclear myosin 1 (NM1) with the genome in mouse embryonic fibroblasts

2015-05-04 | E-GEOD-66542 | biostudies-arrayexpress

BAP1 constrains pervasive H2AK119ub1 to control the transcriptional potential of the genome [RNA-seq]

Project description:Histone-modifying systems play fundamental roles in gene regulation and the development of multicellular organisms. Histone modifications that are enriched at gene regulatory elements have been heavily studied, but the function of modifications found more broadly throughout the genome remains poorly understood. This is exemplified by histone H2A monoubiquitylation (H2AK119ub1), which is enriched at Polycomb-repressed gene promoters but also covers the genome at lower levels. Here, using inducible genetic perturbations and quantitative genomics, we found that the BAP1 deubiquitylase plays an essential role in constraining H2AK119ub1 throughout the genome. Removal of BAP1 leads to pervasive genome-wide accumulation of H2AK119ub1, which causes widespread reductions in gene expression. We show that elevated H2AK119ub1 preferentially counteracts Ser5 phosphorylation on the C-terminal domain of RNA polymerase II at gene regulatory elements and causes reductions in transcription and transcription-associated histone modifications. Furthermore, failure to constrain pervasive H2AK119ub1 compromises Polycomb complex occupancy at a subset of Polycomb target genes, which leads to their derepression, providing a potential molecular rationale for why the BAP1 ortholog in Drosophila has been characterized as a Polycomb group gene. Together, these observations reveal that the transcriptional potential of the genome can be modulated by regulating the levels of a pervasive histone modification.

2021-05-03 | GSE161995 | GEO

BAP1 constrains pervasive H2AK119ub1 to control the transcriptional potential of the genome [ATAC-seq]

2021-05-03 | GSE161994 | GEO

BAP1 constrains pervasive H2AK119ub1 to control the transcriptional potential of the genome [ChIP-seq]

2021-05-03 | GSE161993 | GEO

Nuclear myosin 1 contributes to a chromatin landscape compatible with RNA polymerase II transcription activation

2015-05-04 | GSE66542 | GEO