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Chromatin conformation regulates the coordination between DNA replication and transcription

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE99741 | GEO | 2018/02/14

REPOSITORIES: GEO

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Chromatin conformation regulates the coordination between DNA replication and transcription.

Project description:Chromatin is the template for the basic processes of replication and transcription, making the maintenance of chromosomal integrity critical for cell viability. To elucidate how dividing cells respond to alterations in chromatin structure, here we analyse the replication programme of primary cells with altered chromatin configuration caused by the genetic ablation of the HMGB1 gene, or three histone H1 genes. We find that loss of chromatin compaction in H1-depleted cells triggers the accumulation of stalled forks and DNA damage as a consequence of transcription-replication conflicts. In contrast, reductions in nucleosome occupancy due to the lack of HMGB1 cause faster fork progression without impacting the initiation landscape or fork stability. Thus, perturbations in chromatin integrity elicit a range of responses in the dynamics of DNA replication and transcription, with different consequences on replicative stress. These findings have broad implications for our understanding of how defects in chromatin structure contribute to genomic instability.

| S-EPMC5913246 | biostudies-literature

Chromatin conformation regulates the coordination between DNA replication and transcription [array]

Project description:Chromatin is the template for the basic processes of replication and transcription, making the maintenance of chromosomal integrity critical for cell viability. To elucidate how dividing cells respond to alterations in chromatin structure we analysed the replication initiation landscape, elongation kinetics, and timing of primary cells with altered chromatin configuration caused by the genetic ablation of the HMGB1 gene, or triple-KO in three histone H1 genes. We found that loss of chromatin compaction in H1-depleted cells alters dramatically the initiation patterns triggering the accumulation of stalled forks and DNA damage as a consequence of transcription-replication conflicts, whereas reductions in nucleosome content due to the lack of HMGB1 causes faster fork progression without perturbing the initiation landscape or fork stability. Thus, perturbations in the integrity of the chromatin template elicit a range of responses in the dynamics of DNA replication and transcription, with different consequences on replicative stress. These findings have broad implications for our understanding of how defects in chromatin structure, such as those occurring during cellular aging or in some developmental disorders or cancer, contribute to genomic instability.

2018-02-14 | GSE99739 | GEO

Chromatin conformation regulates the coordination between DNA replication and transcription [SNS-Seq]

Project description:Chromatin is the template for the basic processes of replication and transcription, making the maintenance of chromosomal integrity critical for cell viability. To elucidate how dividing cells respond to alterations in chromatin structure we analysed the replication initiation landscape, elongation kinetics, and timing of primary cells with altered chromatin configuration caused by the genetic ablation of the HMGB1 gene, or triple-KO in three histone H1 genes. We found that loss of chromatin compaction in H1-depleted cells alters dramatically the initiation patterns triggering the accumulation of stalled forks and DNA damage as a consequence of transcription-replication conflicts, whereas reductions in nucleosome content due to the lack of HMGB1 causes faster fork progression without perturbing the initiation landscape or fork stability. Thus, perturbations in the integrity of the chromatin template elicit a range of responses in the dynamics of DNA replication and transcription, with different consequences on replicative stress. These findings have broad implications for our understanding of how defects in chromatin structure, such as those occurring during cellular aging or in some developmental disorders or cancer, contribute to genomic instability.

2018-02-14 | GSE99740 | GEO

Chromatin conformation regulates the coordination between DNA replication and transcription

Project description:Chromatin conformation regulates the coordination between DNA replication and transcription

| PRJNA389460 | ENA

Dzip3 regulates developmental genes in mouse embryonic stem cells by reorganizing 3D chromatin conformation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-08 | E-GEOD-71884 | biostudies-arrayexpress

Crosstalk between sumoylation and acetylation regulates p53-dependent chromatin transcription and DNA binding.

Project description:Covalent modification by small ubiquitin-related modifiers (SUMO) regulates p53 transcription activity through an undefined mechanism. Using reconstituted sumoylation components, we purified SUMO-1-conjugated p53 (Su-p53) to near homogeneity. Su-p53 exists in solution as a tetramer and interacts with p300 histone acetyltransferase as efficiently as the unmodified protein. Nevertheless, it fails to activate p53-dependent chromatin transcription because of its inability to bind DNA. With sequential modification assays, we found that sumoylation of p53 at K386 blocks subsequent acetylation by p300, whereas p300-acetylated p53 remains permissive for ensuing sumoylation at K386 and alleviates sumoylation-inhibited DNA binding. While preventing the free form of p53 from accessing its cognate sites, sumoylation fails to disengage prebound p53 from DNA. The sumoylation-deficient K386R protein, when expressed in p53-null cells, exhibits higher transcription activity and binds better to the endogenous p21 gene compared with the wild-type protein. These studies unravel a molecular mechanism underlying sumoylation-regulated p53 function and further uncover a new role of acetylation in antagonizing the inhibitory effect of sumoylation on p53 binding to DNA.

| S-EPMC2683057 | biostudies-literature

Classifying leukemia types with chromatin conformation data

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-02-27 | E-GEOD-55408 | biostudies-arrayexpress

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-13 | GSE169620 | GEO

Global early replication disrupts gene expression and chromatin conformation in a single cell cycle

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-23 | GSE199450 | GEO

DNA replication and transcription programs respond to the same chromatin cues.

Project description:DNA replication is a dynamic process that occurs in a temporal order along each of the chromosomes. A consequence of the temporally coordinated activation of replication origins is the establishment of broad domains (>100 kb) that replicate either early or late in S phase. This partitioning of the genome into early and late replication domains is important for maintaining genome stability, gene dosage, and epigenetic inheritance; however, the molecular mechanisms that define and establish these domains are poorly understood. The modENCODE Project provided an opportunity to investigate the chromatin features that define the Drosophila replication timing program in multiple cell lines. The majority of early and late replicating domains in the Drosophila genome were static across all cell lines; however, a small subset of domains was dynamic and exhibited differences in replication timing between the cell lines. Both origin selection and activation contribute to defining the DNA replication program. Our results suggest that static early and late replicating domains were defined at the level of origin selection (ORC binding) and likely mediated by chromatin accessibility. In contrast, dynamic domains exhibited low ORC densities in both cell types, suggesting that origin activation and not origin selection governs the plasticity of the DNA replication program. Finally, we show that the male-specific early replication of the X chromosome is dependent on the dosage compensation complex (DCC), suggesting that the transcription and replication programs respond to the same chromatin cues. Specifically, MOF-mediated hyperacetylation of H4K16 on the X chromosome promotes both the up-regulation of male-specific transcription and origin activation.

| S-EPMC4079966 | biostudies-literature

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