Genome-wide analysis of replication timing in ESC and 2CLC during 2CLC emergence [transitional]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA561658 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10014868.fastq.gz | Fastqsanger.gz | |||
| SRR10014869.fastq.gz | Fastqsanger.gz | |||
| SRR10014870.fastq.gz | Fastqsanger.gz | |||
| SRR10014871.fastq.gz | Fastqsanger.gz | |||
| SRR10014872.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide analysis of replication timing in ESC and 2CLC
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Project description:The timing of DNA replication is an important developmentally regulated regional property that is correlated with gene expression, chromatin state, GC content, subnuclear structure. These correlations reflect the variable accessibility of origins to a limited pool of initiation factors within different context, and the extent to which changes in replication timing occur during differentiation. Therefore, temporal order of genome replication could be sufficient to identify the cell type. A lot of studies for characterizing DNA replication have been done using many different types of cells, however, the pattern of it in the totipotent cells is still entirely unknown. In this study, we try to understand the molecular basis underlying totipotency by identifying specific DNA replication features found exclusively in totipotent cells.
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Project description:Mouse ESC 46C replication timing has been assessed by repli-chip.
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Project description:Differentiation of mouse embryonic stem cells (mESCs) is accompanied by changes in replication timing. To explore the relationship between replication timing and cell fate transitions, we constructed genome-wide replication-timing profiles of 22 independent mouse cell lines representing 10 stages of early mouse development, and transcription profiles for seven of these stages. Replication profiles were cell-type specific, with 45% of the genome exhibiting significant changes at some point during development that were generally coordinated with changes in transcription. Comparison of early and late epiblast cell culture models revealed a set of lineage-independent early-to-late replication switches completed at a stage equivalent to the post-implantation epiblast, prior to germ layer specification and down-regulation of key pluripotency transcription factors (Oct4/Nanog/Sox2) and coinciding with the emergence of compact chromatin near the nuclear periphery. These changes were conserved in all subsequent lineages and involved a group of irreversibly down-regulated genes, at least some of which were repositioned closer to the nuclear periphery. Importantly, many genomic regions of partially reprogrammed induced pluripotent stem cells (piPSCs) failed to re-establish ESC-specific replication timing and transcription programs. These regions were enriched for lineage-independent early-to-late changes, which in female cells included the inactive X-chromosome. Taken together, we demonstrate that replication-timing changes are extensive during development. Moreover, a distinct set of lineage-independent, early-to-late changes completed in and stably maintained after the post-implantation epiblast stage is difficult to reprogram and therefore coincides with an epigenetic commitment to differentiation prior to germ layer specification. 8 cell lines, with a total of 14 individual replicates (i.e. 6 in duplicates, 2 in single replicates)
2010-05-19 | E-GEOD-17980 | biostudies-arrayexpress
Project description:The timing of DNA replication is an important developmentally regulated regional property that is correlated with gene expression, chromatin state, GC content, subnuclear structure. These correlations reflect the variable accessibility of origins to a limited pool of initiation factors within different context, and the extent to which changes in replication timing occur during differentiation. Therefore, temporal order of genome replication could be sufficient to identify the cell type. Several studies for characterizing DNA replication have been done using many different types of cells, however, the pattern of it in the totipotent cells is still entirely unknown. In this study, we try to understand the molecular basis underlying totipotency by identifying specific DNA replication features found exclusively in totipotent cells.
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Project description:Differentiation of mouse embryonic stem cells (mESCs) is accompanied by changes in replication timing. To explore the relationship between replication timing and cell fate transitions, we constructed genome-wide replication-timing profiles of 22 independent mouse cell lines representing 10 stages of early mouse development, and transcription profiles for seven of these stages. Replication profiles were cell-type specific, with 45% of the genome exhibiting significant changes at some point during development that were generally coordinated with changes in transcription. Comparison of early and late epiblast cell culture models revealed a set of lineage-independent early-to-late replication switches completed at a stage equivalent to the post-implantation epiblast, prior to germ layer specification and down-regulation of key pluripotency transcription factors (Oct4/Nanog/Sox2) and coinciding with the emergence of compact chromatin near the nuclear periphery. These changes were conserved in all subsequent lineages and involved a group of irreversibly down-regulated genes, at least some of which were repositioned closer to the nuclear periphery. Importantly, many genomic regions of partially reprogrammed induced pluripotent stem cells (piPSCs) failed to re-establish ESC-specific replication timing and transcription programs. These regions were enriched for lineage-independent early-to-late changes, which in female cells included the inactive X-chromosome. Taken together, we demonstrate that replication-timing changes are extensive during development. Moreover, a distinct set of lineage-independent, early-to-late changes completed in and stably maintained after the post-implantation epiblast stage is difficult to reprogram and therefore coincides with an epigenetic commitment to differentiation prior to germ layer specification.
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Project description:Faithful DNA replication is essential for genome integrity. Under-replicated DNA leads to chromosome segregation defects, which are reportedly common during embryogenesis. However, DNA replication regulation remains poorly understood in early mammalian embryos. Here, we constructed a single-cell genome-wide DNA replication atlas of pre-implantation mouse embryos and discovered an abrupt replication program switch accompanied by a transient period of genomic instability. In 1- and 2-cell embryos, we observed the complete absence of a replication timing (RT) program, and the entire genome replicated gradually and uniformly using extremely slow-moving forks. In 4-cell embryos, a somatic-cell-like RT program commenced abruptly. However, the fork speed was still slow, S-phase was extended, and SLX4 DNA repair foci increased during G2/M, which was followed by a transient increase in chromosome segregation errors. Importantly, live imaging captured longer S-phase of error cells, and the breakpoints identified by single-cell genome sequencing were enriched in late-replicating regions. By the 8-cell stage, forks gained speed, S-phase was no longer extended, and chromosome aberrations disappeared. Thus, a transient period of genomic instability exists during normal mouse development, which is preceded by a fragile S-phase lacking the coordination between replisome-level regulation and megabase-scale RT regulation, implicating the importance of their coordination for genome integrity.
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