Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA267716 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Distinct classes of genes behave as either drivers or dependents of replication timing switches.
| PRJNA268362 | ENA
Project description:Duplication of the genome in mammalian cells occurs in a defined temporal order referred as its replication-timing program (RT). RT is regulated in units of 400-800 Kb referred as replication domains (RDs) and changes dynamically during development. Changes in RT are generally coordinated with transcriptional competence and changes in sub-nuclear position. We generated genome-wide RT profiles for 29 distinct human cell types including embryonic stem cell (hESC)-derived, primary cells and established cell lines representing intermediate stages of endoderm, mesoderm, ectoderm and neural crest (NC) development. We identified clusters of RDs that replicate at unique times in each stage (RT signatures). Surprisingly, transcriptome data revealed that, despite an overall correlation between early replication and transcriptional activity, most genes that switched RT during differentiation can be expressed when late replicating. Intriguingly, this class of genes was nonetheless induced to high expression levels prior to a late to early RT switch and down-regulated after the switch back to late replication. These results clarify the complex relationship between transcription and RT and identify classes of genes that behave as potential drivers of the RT switch vs. those that may depend upon an RT switch for transcriptional induction. Genome-wide replication timing profiles were constructed from 60 human samples covering 29 distinct cell types including embryonic stem cell (hESC)-derived, primary cells and established cell lines representing intermediate stages of endoderm, mesoderm, ectoderm and neural crest (NC) development.
2015-05-28 | E-GEOD-63428 | biostudies-arrayexpress
Project description:Duplication of the genome in mammalian cells occurs in a defined temporal order referred as its replication-timing program (RT). RT is regulated in units of 400-800 Kb referred as replication domains (RDs) and changes dynamically during development. Changes in RT are generally coordinated with transcriptional competence and changes in sub-nuclear position. We generated genome-wide RT profiles for 29 distinct human cell types including embryonic stem cell (hESC)-derived, primary cells and established cell lines representing intermediate stages of endoderm, mesoderm, ectoderm and neural crest (NC) development. We identified clusters of RDs that replicate at unique times in each stage (RT signatures). Surprisingly, transcriptome data revealed that, despite an overall correlation between early replication and transcriptional activity, most genes that switched RT during differentiation can be expressed when late replicating. Intriguingly, this class of genes was nonetheless induced to high expression levels prior to a late to early RT switch and down-regulated after the switch back to late replication. These results clarify the complex relationship between transcription and RT and identify classes of genes that behave as potential drivers of the RT switch vs. those that may depend upon an RT switch for transcriptional induction.
2015-05-28 | GSE63428 | GEO
Project description:Duplication of the genome in mammalian cells occurs in a defined temporal order referred as its replication-timing program (RT). RT is regulated in units of 400-800 Kb referred as replication domains (RDs) and changes dynamically during development. Changes in RT are generally coordinated with transcriptional competence and changes in sub-nuclear position. We generated genome-wide RT profiles for 29 distinct human cell types including embryonic stem cell (hESC)-derived, primary cells and established cell lines representing intermediate stages of endoderm, mesoderm, ectoderm and neural crest (NC) development. We identified clusters of RDs that replicate at unique times in each stage (RT signatures). Surprisingly, transcriptome data revealed that, despite an overall correlation between early replication and transcriptional activity, most genes that switched RT during differentiation can be expressed when late replicating. Intriguingly, this class of genes was nonetheless induced to high expression levels prior to a late to early RT switch and down-regulated after the switch back to late replication. These results clarify the complex relationship between transcription and RT and identify classes of genes that behave as potential drivers of the RT switch vs. those that may depend upon an RT switch for transcriptional induction.
2015-06-03 | GSE63592 | GEO
Project description:Differentiation of mouse embryonic stem cells (mESCs) is accompanied by global changes in replication timing. To elucidate this reorganization process and explore its potential impact on mouse development, we constructed genome-wide replication-timing profiles of 15 independent mouse cell types representing nine different stages of early mouse development, including all three germ layers. Overall, 45% of the genome exhibits significant changes in replication timing between cell types, indicating that replication-timing regulation is more extensive than previously estimated from neural differentiation. Intriguingly, analysis of early and late epiblast cell culture models suggest that the earliest changes in development include extensive lineage-independent early-to-late replication switches that are 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). These changes were stable in all subsequent lineages and involved a class of irreversibly silenced genes that were re-positioned closer to the nuclear periphery. Lineage-specific, late-to-early and early-to-late replication switches followed, which created cell-type specific replication profiles. Importantly, partially reprogrammed induced pluripotent stem cells (piPSCs) failed to restore ESC-specific replication timing and transcription programs particularly within regions of lineage-independent early-to-late replication changes, as well as the inactive X-chromosome. We conclude that lineage-independent, early-to-late replication-timing switches that occur in the post-implantation epiblast embody an epigenetic commitment to differentiation prior to germ layer specification. 22 cell lines, with a total of 36 individual replicates (i.e. 14 in duplicates, 8 in single replicates)
2010-05-19 | E-GEOD-17983 | biostudies-arrayexpress
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Differentiation of mouse embryonic stem cells (mESCs) is accompanied by global changes in replication timing. To elucidate this reorganization process and explore its potential impact on mouse development, we constructed genome-wide replication-timing profiles of 15 independent mouse cell types representing nine different stages of early mouse development, including all three germ layers. Overall, 45% of the genome exhibits significant changes in replication timing between cell types, indicating that replication-timing regulation is more extensive than previously estimated from neural differentiation. Intriguingly, analysis of early and late epiblast cell culture models suggest that the earliest changes in development include extensive lineage-independent early-to-late replication switches that are 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). These changes were stable in all subsequent lineages and involved a class of irreversibly silenced genes that were re-positioned closer to the nuclear periphery. Lineage-specific, late-to-early and early-to-late replication switches followed, which created cell-type specific replication profiles. Importantly, partially reprogrammed induced pluripotent stem cells (piPSCs) failed to restore ESC-specific replication timing and transcription programs particularly within regions of lineage-independent early-to-late replication changes, as well as the inactive X-chromosome. We conclude that lineage-independent, early-to-late replication-timing switches that occur in the post-implantation epiblast embody an epigenetic commitment to differentiation prior to germ layer specification.
2009-11-25 | GSE17983 | GEO
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:Anticancer properties of distinct antimalaria drug classes
| PRJNA224735 | ENA