Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153283 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Here we map the localization of Mod(mdg4), including Mod(mdg4)2.2 specific and Mod(mdg4) common to all isoforms, to chromatin insulators, as well as the lethal-3 malignant brain tumor protein in Drosophila Kc cells. examination of genomic occupancy for Mod(mdg4)2.2, Mod(mdg4)BTB (all isoforms), and L(3)mbt, control samples used for Drosophila Kc were previously described (Wood, Van Bortle et al., 2011 GSE30740)
2012-06-18 | E-GEOD-36393 | biostudies-arrayexpress
Project description:Here we map the localization of Mod(mdg4), including Mod(mdg4)2.2 specific and Mod(mdg4) common to all isoforms, to chromatin insulators, as well as the lethal-3 malignant brain tumor protein in Drosophila Kc cells.
2012-06-18 | GSE36393 | GEO
Project description:Distribution of Drosophila insulator proteins after ecdysone treatment in Kc cells
| PRJNA154553 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE30686: Gene expression analysis of Kc cells from Drosophila melanogaster during ecdysone treatment and CP190 knockdown GSE30740: Distribution of Drosophila insulator proteins after ecdysone treatment in Kc cells Refer to individual Series
2011-10-13 | E-GEOD-30741 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE15660: Gene Expression analysis of Kc and Mbn2 cell lines from Drosophila melanogaster. GSE15661: Genome-wide binding profiles of Drosophila melanogaster insulator proteins in Kc and Mbn2 cells (Set1) GSE15662: Genome-wide binding profiles of Drosophila melanogaster insulator proteins in Kc and Mbn2 cells (Set2) GSE15663: Genome-wide binding profiles of Drosophila melanogaster insulator proteins in Kc and Mbn2 cells (Set3) Refer to individual Series
2010-05-19 | E-GEOD-15664 | biostudies-arrayexpress
Project description:The asynchronous timing of replication of different chromosome domains is essential for eukaryotic genome stability, but the mechanisms establishing replication timing programs remain incompletely understood. Drosophila SNF2-related factor SUUR imparts under-replication (UR) of late-replicating intercalary heterochromatin (IH) domains in polytene chromosomes. SUUR negatively regulates DNA replication fork progression across IH; however, its mechanism of action remains obscure. Here we developed a novel method termed MS-Enabled Rapid protein Complex Identification (MERCI) to isolate a stable stoichiometric native complex SUMM4 that comprises SUUR and a chromatin boundary protein Mod(Mdg4)-67.2. In vitro, Mod(Mdg4) stimulates the ATPase activity of SUUR, although neither SUUR nor SUMM4 can remodel nucleosomes. Mod(Mdg4)-67.2 and SUUR distribution patterns in vivo partially overlap, and Mod(Mdg4) is required for a normal spatiotemporal distribution of SUUR in chromosomes. SUUR and Mod(Mdg4)-67.2 mediate insulator activities of the gypsy mobile element that disrupt enhancer-promoter interactions and establish euchromatin-heterochromatin barriers in the genome. Furthermore, mutations of SuUR or mod(mdg4) reverse the locus-specific UR. These findings reveal that DNA replication can be delayed by a chromatin barrier and thus, uncover a critical role for architectural proteins in replication timing control. They also provide a biochemical link between ATP-dependent motor factors and the activity of insulators in regulation of gene expression and chromatin partitioning.
2022-12-04 | GSE189421 | GEO
Project description:Distribution of insulator proteins CP190, dCTCF, Su(Hw) and Mod(mdg4)2.2 in Drosophila S2 cells in the presence or absence of dPARP inhibitor 3AB
| PRJNA176855 | ENA
Project description:Distribution of Drosophila insulator proteins DREF in Drosophila Kc167 cells
| PRJNA171353 | ENA
Project description:In Drosophila, defects in asymmetric cell division can result in the formation of stem cell derived tumors. Here, we reveal a different mechanism that can result in the formation of very similar terminal brain tumor phenotypes. We demonstrate that brain tumors in l(3)mbt mutants originate from overproliferation of neuroepithelial cells in the optic lobes caused by de-repression of target genes in the Salvador-Warts-Hippo (SWH) pathway. We use ChIP-seq to identify L(3)mbt-binding sites and show that L(3)mbt binds to chromatin insulator elements. Mutating l(3)mbt or inhibiting the insulator protein mod(mdg4) results in upregulation of SWH pathway reporters. As l(3)mbt tumors are rescued by mutations in bantam or yorkie or by overexpression of expanded the deregulation of SWH pathway target genes is an essential step in brain tumor formation. Our data reveal that very different primary defects can result in the formation of brain tumors, which behave quite similarly in their advanced stages.
2011-08-29 | GSE29206 | GEO
Project description:Distribution of Drosophila insulator proteins during interphase and mitosis
| PRJNA147079 | ENA