Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167951 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR503482_1.fastq.gz | Fastqsanger.gz | |||
| SRR503482_2.fastq.gz | Fastqsanger.gz | |||
| SRR503483_1.fastq.gz | Fastqsanger.gz | |||
| SRR503483_2.fastq.gz | Fastqsanger.gz | |||
| SRR503484_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Chromodomains are found in many regulators of chromatin structure. Most of them recognize methylated histones. Here, we investigate the role of the Corto chromodomain. This Drosophila melanogaster Enhancer of Polycomb and Trithorax is involved in both silencing and activation of gene expression. Overexpression of Corto chromodomain (CortoCD) in transgenic flies show that this domain is critical for Corto function and behaves as a chromatin-targeting module. Mass spectrometry analysis of peptides pulled down by CortoCD from nuclear extracts reveals that they correspond to nuclear ribosomal proteins (RPs). Notably, CortoCD binds with high affinity RPL12 tri-methylated on lysine 3 (RPL12K3me3) as demonstrated by real-time interaction analyses. Co-localization of Corto and RPL12 with active epigenetic marks on polytene chromosomes suggests that they are involved in fine-tuning transcription of genes located in open chromatin. Hence, pseudo-ribosomal complexes composed of various RPs might participate in regulation of gene expression in connection with chromatin regulators. RNA-seq analysis of wing imaginal discs overexpressing either Corto or RPL12 show that most deregulated genes are shared by both factors. Interestingly, these common targets are enriched in RP genes suggesting that Corto and RPL12 are involved in dynamic coordination of ribosome biogenesis.
2012-09-05 | GSE38435 | GEO
Project description:Chromodomains are found in many regulators of chromatin structure. Most of them recognize methylated histones. Here, we investigate the role of the Corto chromodomain. This Drosophila melanogaster Enhancer of Polycomb and Trithorax is involved in both silencing and activation of gene expression. Overexpression of Corto chromodomain (CortoCD) in transgenic flies show that this domain is critical for Corto function and behaves as a chromatin-targeting module. Mass spectrometry analysis of peptides pulled down by CortoCD from nuclear extracts reveals that they correspond to nuclear ribosomal proteins (RPs). Notably, CortoCD binds with high affinity RPL12 tri-methylated on lysine 3 (RPL12K3me3) as demonstrated by real-time interaction analyses. Co-localization of Corto and RPL12 with active epigenetic marks on polytene chromosomes suggests that they are involved in fine-tuning transcription of genes located in open chromatin. Hence, pseudo-ribosomal complexes composed of various RPs might participate in regulation of gene expression in connection with chromatin regulators. RNA-seq analysis of wing imaginal discs overexpressing either Corto or RPL12 show that most deregulated genes are shared by both factors. Interestingly, these common targets are enriched in RP genes suggesting that Corto and RPL12 are involved in dynamic coordination of ribosome biogenesis. To address the role of Corto and RPL12 in regulation of transcription, we deep-sequenced transcripts of wing imaginal discs from third instar larvae over-expressing either FH-cortoCD or RpL12-Myc under control of the wing-specific scalloped::Gal4 driver (sd::Gal4>UAS::FH-cortoCD or sd::Gal4>UAS::RpL12-Myc). Total RNA from FH-cortoCD or RpL12-Myc, the sd::Gal4/+ control or a w1118 reference line were isolated from pools of wing imaginal discs and subjected to RNA-seq on an Illumina high throughput sequencer.
2012-09-05 | E-GEOD-38435 | biostudies-arrayexpress
Project description:Polycomb-directed repression of gene expression is frequently misregulated in human diseases. A quantitative and target-specific cellular assay was utilized to discover the first potent positive allosteric modulator (PAM) peptidomimetic, UNC4976, of nucleic acid binding by CBX7, a chromodomain methyl-lysine reader of Polycomb repressive complex 1. The PAM activity of UNC4976 resulted in enhanced efficacy across three orthogonal cellular assays by simultaneously antagonizing H3K27me3-specific recruitment of CBX7 to target genes while increasing non-specific binding to DNA and RNA. PAM activity thereby reequilibrates PRC1 away from H3K27me3 target regions. Together, our discovery and characterization of UNC4976 not only revealed the most cellularly potent PRC1-specific chemical probe to date, but also uncovers a potential mechanism of Polycomb regulation with implications for non-histone lysine methylated interaction partners.
2019-08-13 | GSE135762 | GEO
Project description:Comparing active and repressed expression states of genes controlled by the Polycomb/Trithorax group proteins
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Project description:The antagonistic actions of Polycomb and Trithorax are responsible for proper cell fate determination in mammalian tissues. In the epidermis, a self-renewing epithelium, previous work has shown that release from Polycomb repression only partially explains differentiation gene activation. We now show that Trithorax is also a key regulator of epidermal differentiation, not only through activation of genes repressed by Polycomb in progenitor cells, but also through activation of genes independent of regulation by Polycomb. The differentiation associated transcription factor GRHL3/GET1 recruits the ubiquitously expressed Trithorax complex to a subset of differentiation genes.
2012-11-10 | GSE42180 | GEO
Project description:A strand-specific switch in noncoding transcription switches the function of a Polycomb/Trithorax response element
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Project description:The antagonistic actions of Polycomb and Trithorax are responsible for proper cell fate determination in mammalian tissues. In the epidermis, a self-renewing epithelium, previous work has shown that release from Polycomb repression only partially explains differentiation gene activation. We now show that Trithorax is also a key regulator of epidermal differentiation, not only through activation of genes repressed by Polycomb in progenitor cells, but also through activation of genes independent of regulation by Polycomb. The differentiation associated transcription factor GRHL3/GET1 recruits the ubiquitously expressed Trithorax complex to a subset of differentiation genes. Examination of WDR5 and GRHL3 binding in human differentited primary keratinocytes (NHEK). High calcium medium was added to NHEK cells at 50% confluency to induce differentiation. Cells were collected for ChIP 24 hours after addition of high calcium medium. ChIP with Wdr5 and Grhl3 antibodies, and an input control were sequenced.
2012-11-10 | E-GEOD-42180 | biostudies-arrayexpress
Project description:The POLYCOMB proteins are required for maintenance of silent chromatin states mediated by H3K27 trimethylation in animals, but POLYCOMB homologues are not found in plant genomes. Using DamID-chip, we found that the Arabidopsis chromodomain-containing protein LHP1 localizes to chromatin associated with H3K27me3 genome-wide. Furthermore, the LHP1 chromodomain binds H3K27me3 with high affinity. These results suggest that LHP1 shares similar functions with POLYCOMB. Keywords: DamID-Chip
2007-09-07 | GSE8169 | GEO
Project description:Tight control over cell identity gene expression is necessary for proper adult form and function. The opposing activities of Polycomb and trithorax complexes determine the ON/OFF state of targets like the Hox genes. Trithorax encodes a methyltransferase specific to histone H3 lysine-4 (H3K4). However, there is no direct evidence that H3K4 regulates Polycomb group target genes in vivo. Here, we demonstrate two key roles for replication-dependent histone H3.2K4 in target control. We find that H3.2K4 antagonizes Polycomb group catalytic activity and that it is required for proper target gene activation. We conclude that H3.2K4 directly regulates expression of Polycomb targets.
2024-12-18 | GSE273885 | GEO
Project description:The transcriptional activating and repressive functions performed by Trithorax and Polycomb group complexes, respectively, are critical for to maintain cellular fates in ontogeny and in cancer. Here we report that leukemias initiated by a Trithorax-related oncogene, MLL-AF9, depend upon the Polycomb Repressive Complex 2 (PRC2) to sustain a transformed cellular state. RNAi mediated suppression of PRC2 subunits is sufficient to inhibit proliferation of MLL-AF9 leukemias, with little impact on growth of non-transformed cells. This requirement is partly due to PRC2-mediated transcriptional repression of several anti-self-renewal regulators, including Cdkn2a. These results suggest that, unlike the classical antagonism generally observed between Polycomb and Trithorax group proteins during development, the activities of these two pathways can cooperate to promote myeloid neoplasia.
2013-07-01 | GSE34183 | GEO