Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323936 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3609453.fastq.gz | Fastqsanger.gz | |||
| SRR3609454.fastq.gz | Fastqsanger.gz |
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Project description:Although histone modifications have been implicated in many DNA-dependent processes, their precise role in DNA replication remains poorly understood. Here, we show that the regulation of histone H4-K20 methylation states, in particular for the trimethylation, is a critical determinant of licensing and time activation of replication origins in mammalian cells.
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Project description:Although histone modifications have been implicated in many DNA-dependent processes, their precise role in DNA replication remains poorly understood. Here, we show that the regulation of histone H4-K20 methylation states, in particular for the monomethylation, is a critical determinant of licensing and time activation of replication origins in mammalian cells.
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Project description:Although histone modifications have been implicated in many DNA-dependent processes, their precise role in DNA replication remains poorly understood. Here, we show that the regulation of histone H4-K20 methylation states, in particular for the monomethylation, is a critical determinant of licensing and time activation of replication origins in mammalian cells. Two experimental condition : shRNA LUC cells (control) versus siRNA Prset-7 cells
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Project description:Although histone modifications have been implicated in many DNA-dependent processes, their precise role in DNA replication remains poorly understood. Here, we show that the regulation of histone H4-K20 methylation states, in particular for the trimethylation, is a critical determinant of licensing and time activation of replication origins in mammalian cells. WT cells versus suv4-20h KO cells, and non-induced cells versus induced cells
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Project description:DNA replication ensures the accurate transmission of genetic information during cell cycle. The interaction between histone methyltransferase SUV420H1 and histone variant H2A.Z plays a critical role in the licensing of early replication origins. However, the mechanism by which SUV420H1 preferentially recognizes H2A.Z-nucleosome and deposits H4 lysine 20 dimethylation (H4K20me2) on DNA replication origins remains elusive. Here, we determined the cryo-EM structures of SUV420H1 bound to H2A.Z-nucleosome or H2A-nucleosome. Our structures show that the SUV420H1 catalytic domain (CD) directly interacts with histone H4 and nucleosomal DNA, whereas a SUV420H1 arginine-rich motif (ARM) anchors to the acidic patch of the nucleosome. The N-terminal aminal acid residues of H4 (Aa 1-24) forms a lasso-shaped structure sandwiched between SUV420H1 CD and nucleosome. The lasso-shaped structure stabilizes the SUV420H1-nucleosome interaction and precisely projects the H4 K20 residue into the SUV420H1 catalytic center. Further analyses revealed a crucial role of SUV420H1 KR-loop (aminal acid residues 214-223), which spatially lies closely to H2A.Z specific residues D97/S98, in dictating the preference for H2A.Z-nucleosome. SUV420H1 K219A/R220A mutations reduced the activity of SUV420H1 for H4K20me2 modification, the preference of SUV420H1 for H2A.Z-nucleosome, and the efficiency of DNA replication initiation. Collectively, our findings elucidate how SUV420H1 preferentially recognizes H2A.Z-nucleosome to deposit H4K20me2 modification and shed light on therapeutic strategies targeting the DNA replication initiation.
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Project description:Mammalian DNA replication starts at distinct chromosomal sites in a tissue-specific pattern coordinated with transcription, but previous studies have not yet identified a chromatin modification that correlates with the initiation of DNA replication. This submission is associated with a paper in which we report that replication initiation events are associated with a high frequency of methylation of histone H3 on lysine K79 (H3K79Me2 and H3K79Me3). H3K79Me2-containing chromatin exhibited the highest enrichment of replication initiation events observed in a single chromatin modification. Importantly, H3K79 methylation was enriched in chromatin containing a replicator (a DNA sequence capable of initiating DNA replication), but not in chromatin containing a mutant replicator that could not initiate replication. The association of H3K79Me2 with replication initiation sites was independent and not synergistic with other chromatin modifications. H3K79 methylation exhibited a wider distribution and greater abundance during S-phase, but regions of chromatin that were only modified during S-phase were not enriched in replication initiation events. In addition, the paper shows that depletion of DOT1L, the sole enzyme responsible for H3K79 methylation, triggered limited genomic over-replication. These data are consistent with the hypothesis that methylation of H3K79 associates with replication origins and marks replicated chromatin during S-phase to prevent re-replication and preserve genomic stability. Evaluation of HeK79 methylation in chromatin samples from cell cycle fractionated K562 leukemia cells. Unsyncrhonized untreated cultures of K562 cells were fractionated by size using centrifugal elutriation. Chromatin was isolated and subject to ChIP-Seq with antibodies directed against dimethylated and trimethylated lysine on histone H3.
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Project description:Mammalian chromosome replication starts from distinct sites, but the principles governing initiation site selection are unclear because proteins essential for DNA replication do not exhibit sequence-specific DNA binding. We identified a replication initiation determinant (RepID) protein that binds a subset of replication initiation sites. A large fraction of RepID binding sites share a common G-rich motif and exhibit elevated replication initiation. RepID is required for initiation of DNA replication from Rep-ID bound replication origins, including the origin at the human beta-globin (HBB) locus. At HBB, RepID is involved in an interaction between the replication origin (Rep-P) and the locus control region. RepID depleted murine embryonic fibroblasts exhibit abnormal replication fork progression and fewer replication initiation events. These observations are consistent with a model suggesting that RepID facilitates replication initiation at a distinct group of human replication origins.
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Project description:Mammalian chromosome replication starts from distinct sites, but the principles governing initiation site selection are unclear because proteins essential for DNA replication do not exhibit sequence-specific DNA binding. We identified a replication initiation determinant (RepID) protein that binds a subset of replication initiation sites. A large fraction of RepID binding sites share a common G-rich motif and exhibit elevated replication initiation. RepID is required for initiation of DNA replication from Rep-ID bound replication origins, including the origin at the human beta-globin (HBB) locus. At HBB, RepID is involved in an interaction between the replication origin (Rep-P) and the locus control region. RepID depleted murine embryonic fibroblasts exhibit abnormal replication fork progression and fewer replication initiation events. These observations are consistent with a model suggesting that RepID facilitates replication initiation at a distinct group of human replication origins. Nascent strands were purified with the lambda exonuclease methods from HCT116 cells and sequenced. Chromatin from unsyncrhonized untreated cultures of U2OS cells was subjected to ChIP-Seq with antibody directed against RepID/PHIP
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Project description:Duplication of eukaryotic genomes during S phase is coordinated in space and time. In order to identify zones of initiation and cell-type as well as gender-specific plasticity of DNA replication, we profiled replication timing, histone acetylation and transcription throughout the Drosophila genome. We observed two waves of replication initiation with many distinct zones firing in early and multiple, less defined peaks at the end of S phase, suggesting that initiation becomes more promiscuous at the end of S phase. A comparison of different cell types revealed widespread plasticity of replication timing on autosomes. Most occur in large regions but only half coincide with local differences in transcription. In contrast to confined autosomal differences, a global shift in replication timing occurs throughout the single male X chromosome. Unlike in females, the dosage compensated X chromosome replicates almost exclusively early. This difference occurs at sites which are not transcriptionally hyperactivated, but show increased acetylation of lysine 16 of histone H4. This suggests a transcription-independent, yet chromosome-wide process related to chromatin. Importantly, H4K16ac is also enriched at initiation zones as well as early replicating regions on autosomes during S phase. Together, our data reveal novel organizational principles of DNA replication of the Drosophila genome and imply chromatin structure as a determinant of replication timing locally and chromosome-wide. Keywords: cell type comparison, chip-chip, replication timing
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