Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA242311 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CGH of stage 13 amplifying follicle cells to measure changes in replication fork progression in double-strand break repair mutants Comparative genomic hybridization was performed to compare amplification gradients of stage 13 follicle cells from several double-strand break repair mutants to wild type (OrR) gradients. Two-three replicates were done for each genotype.
2017-02-08 | GSE86012 | GEO
Project description:Comparative genomic hybridization was performed to compare amplificaiton gradients in genomic DNA derived from stage 13 egg chambers of wild-type, suppressor of under-replication (SuUR) mutant and SuUR overexpression, compared with 0-2hr diploid embryo gDNA. Comparative genomic hybridization was performed to compare amplificaiton gradients in genomic DNA derived from stage 10B egg chambers of wild-type, compared with 0-2hr diploid embryo gDNA.
2014-11-10 | GSE56054 | GEO
Project description:Control of DNA copy number is essential to maintain genome stability and ensure proper cell and tissue function. In Drosophila, the SNF2-domain-containing SUUR protein inhibits replication fork progression within specific regions of the genome to promote DNA underreplication. While dissecting the function of SUUR’s SNF2 domain, we identified a physical interaction between SUUR and Rif1. Rif1 has many roles in DNA metabolism and regulates the replication timing program. We demonstrate that repression of DNA replication is dependent on Rif1. Rif1 localizes to active replication forks in an SUUR-dependent manner and directly regulates replication fork progression. Importantly, SUUR associates with replication forks in the absence of Rif1, indicating that Rif1 acts downstream of SUUR to inhibit fork progression. Our findings uncover an unrecognized function of the Rif1 protein as a direct regulator of replication fork progression suggesting developmental regulation of Rif1 activity.
2018-10-15 | GSE114370 | GEO
Project description:We analyzed gamma-H2Av ChIP-Seq from hand dissected salivary glands of wandering third instar larvae from wild-type (OrR) or suppressor of under-replication (SuUR) mutant Drosophila. Goals were to determine the DNA damage profile relative to underreplicated domains. We analyzed SUUR and Cdc45 ChIP-Seq from hand dissected early (stage 10) and late (stage 12/13) egg chambers from adult Drosophila ovaries. The goals was to determine the localization of SUUR relative to replication forks.
2014-11-10 | GSE55932 | GEO
Project description:CGH of stage 13 amplifying follicle cells to measure changes in replication fork progression in DNA damage checkpoint and double-strand break repair mutants
| PRJNA277728 | ENA
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:We analyzed gamaH2Av ChIP-seq from hand dissected stage 10B and 13 follicle cell nuclei. Egg chambers were dissected from wild-type (OrR) or H2Av[ΔCT] ovaries to assess binding at the Drosophila Follicle Cell Amplicons and across the genome. ChIP-seq of gammaH2Av bound to follicle cell DNA from stage 10B and 13 egg chambers, collected from wild-type (OrR) and H2Av[ΔCT] Drosophila ovaries. Sequences analyzed by Illumina sequencing. Two replicates are included for each ChIP reaction.
2015-06-18 | E-GEOD-66689 | biostudies-arrayexpress
Project description:Regulation of DNA replication and copy number are necessary to promote genome stability and maintain cell and tissue function. DNA replication is regulated temporally in a process known as replication timing (RT). Rif1 is key regulator of RT and has a critical function in copy number control in polyploid cells. In a previous study (Munden et al., 2018), we demonstrated that Rif1 functions with SUUR to inhibit replication fork progression and promote underreplication of specific genomic regions. How Rif1-dependent control of RT factors into its ability to promote underreplication is unknown. By applying a computational approach to measure RT in Drosophila polyploid cells, we show that SUUR and Rif1 have differential roles in controlling underreplication and RT. Our findings reveal that Rif1 functions both upstream and downstream of SUUR to promote underreplication. Our work provides new mechanistic insight into the process of underreplication and its links to RT.
2021-09-02 | GSE172375 | GEO
Project description:We analyzed gamaH2Av ChIP-seq from hand dissected stage 10B and 13 follicle cell nuclei. Egg chambers were dissected from wild-type (OrR) or H2Av[ΔCT] ovaries to assess binding at the Drosophila Follicle Cell Amplicons and across the genome.
2015-06-18 | GSE66689 | GEO
Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature – in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal.
2016-01-10 | GSE74907 | GEO