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Preferential re-replication of Drosophila heterochromatin

ABSTRACT: DNA copy number profile of Drosophila Kc167 cells comparing control pUC dsRNA treated cells and geminin dsRNA treated cells.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE20932 | GEO | 2010/03/18

SECONDARY ACCESSION(S): PRJNA124375

REPOSITORIES: GEO

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Preferential re-replication of Drosophila heterochromatin

Project description:DNA copy number profile of Drosophila Kc167 cells comparing control pUC dsRNA treated cells and geminin dsRNA treated cells. CGH: 2 controls, 2 geminin knockdowns, 2 platforms

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Preferential re-replication of Drosophila heterochromatin in the absence of geminin.

Project description:To ensure genomic integrity, the genome must be duplicated exactly once per cell cycle. Disruption of replication licensing mechanisms may lead to re-replication and genomic instability. Cdt1, also known as Double-parked (Dup) in Drosophila, is a key regulator of the assembly of the pre-replicative complex (pre-RC) and its activity is strictly limited to G1 by multiple mechanisms including Cul4-Ddb1 mediated proteolysis and inhibition by geminin. We assayed the genomic consequences of disregulating the replication licensing mechanisms by RNAi depletion of geminin. We found that not all origins of replication were sensitive to geminin depletion and that heterochromatic sequences were preferentially re-replicated in the absence of licensing mechanisms. The preferential re-activation of heterochromatic origins of replication was unexpected because these are typically the last sequences to be duplicated in a normal cell cycle. We found that the re-replication of heterochromatin was regulated not at the level of pre-RC activation, but rather by the formation of the pre-RC. Unlike the global assembly of the pre-RC that occurs throughout the genome in G1, in the absence of geminin, limited pre-RC assembly was restricted to the heterochromatin by elevated cyclin A-CDK activity. These results suggest that there are chromatin and cell cycle specific controls that regulate the re-assembly of the pre-RC outside of G1.

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The effects of PTIP on Polycomb mediated repression in Drosophila Kc167 cells.

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SPOP mutation induces replication over-firing by impairing Geminin ubiquitination and triggers replication catastrophe upon ATR inhibition

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Project description:Drosophila Kc167 cells were used to test the function of PTIP in regulating gene expression before and after loss of polycomb function. Four condtions were tested using dsRNA knockdowns (RNAi) Experiment Overall Design: Kc167 cells alone, Kc cells with loss of PTIP, cells with loss of polycomb and polyhomeotic, and cells with loss of PTIP, polycomb, and polyhomeotic. Performed in triplicate.

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Project description:The replication of the genome is a highly organized process, both spatially and temporally. Although a lot is known on the composition of the basic replication machinery, how its activity is regulated is mostly unknown. Several chromatin properties have been proposed as regulators, but a potential role of the nuclear DNA position remains unclear. We made use of the prominent structure and well-defined heterochromatic landscape of mouse pericentric chromosome domains as a well-studied example of late replicating constitutive heterochromatin. We established a method to manipulate its nuclear position and evaluated the effect on replication timing, DNA compaction and epigenetic composition. Using time-lapse microscopy, we observed that constitutive heterochromatin, known to replicate during late S-phase, was replicated in mid S-phase when repositioned to the nuclear periphery. Out-of-schedule replication resulted in deficient post-replicative maintenance of chromatin modifications, namely silencing marks. We propose that repositioned constitutive heterochromatin was activated in trans according to the domino model of origin firing by nearby (mid S) firing origins. In summary, our data provide, on the one hand, a novel approach to manipulate nuclear DNA position and, on the other hand, establish nuclear DNA position as a novel mechanism regulating DNA replication timing and epigenetic maintenance.

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Kc167 Replication Origins

Project description:modENCODE_submission_709 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Early origins of replication were identified by treating cells with hydroxyurea (HU), a potent inhibitor of nucleotide synthesis, in the presence of the nucleotide analogue BrdU. Treatment of synchronized Kc167 cells with HU stalls replication forks and activates the intra S-phase checkpoint, thereby limiting BrdU incorporation to those sequences immediately adjacent to early activating replication origins. BrdU enriched sequences surrounding early origins of replication are then enriched by immunoprecipitation with an anti-BrdU antibody. Early origins are then detected by hybridization to Agilent genomic tiling arrays. Peaks are called using MA2C (http://liulab.dfci.harvard.edu/MA2C/MA2C.htm) Keywords: CHIP-chip For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: Kc167; Tissue: embryo-derived cell-line; Genotype: se/e; Sex: Female NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Cell Line Kc167

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