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LaminB1 DamID, RNA-seq and Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

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

ORGANISM(S): Mus musculus

PROVIDER: GSE262791 | GEO | 2025/03/18

REPOSITORIES: GEO

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LaminB1 DamID analysis in RIF1 depleted preimplantation mouse embryos

Project description:We investigated how RIF1 depletion affects the nuclear organization in mouse preimplantation embryos by performing DamID-seq to map lamina-associated domains (LADs).

2025-03-18 | GSE262788 | GEO

Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

Project description:Repli-seq datasets were generated using single cell Repli-seq as described in Nakatani et al. (2024). Embryos were microinjected with an siRNA control or an siRNA against Rif1 at the zygote stage. Individual cells were collected for scRepli-seq at the 4-cell, 8-cell and Morula stage embryos.

2025-03-18 | GSE262790 | GEO

LaminB1 DamID analysis in RIF1 depleted preimplantation mouse embryos

Project description:LaminB1 DamID analysis in RIF1 depleted preimplantation mouse embryos

| PRJNA1093387 | ENA

LaminB1 DamID, RNA-seq and Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

Project description:LaminB1 DamID, RNA-seq and Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

| PRJNA1093385 | ENA

Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

Project description:Genome-wide analysis of replication timing in RIF1 depleted preimplantation mouse embryos

| PRJNA1093388 | ENA

Genome-wide analysis of replication timing in preimplantation mouse embryos

Project description:Replication timing is cell type specific, is tightly linked to the 3D nuclear organisation of the genome and is considered an epigenetic fingerprint. In spite of its importance in maintaining the epigenome the developmental regulation of replication timing in mammals in vivo has not been explored. Here, using single cell Repli-seq, we generated the genome-wide replication timing maps of mouse embryos from the zygote until the blastocyst stage.

2023-10-16 | GSE218365 | GEO

Rif1 regulates the replication timing domains on the human genome.

Project description:DNA replication is spatially and temporally regulated during S-phase. DNA replication timing is established in early-G1-phase at a point referred to as timing decision point. However, how the genome-wide replication timing domains are established is unknown. Here, we show that Rif1 (Rap1-interacting-factor-1), originally identified as a telomere-binding factor in yeast, is a critical determinant of the replication timing programme in human cells. Depletion of Rif1 results in specific loss of mid-S replication foci profiles, stimulation of initiation events in early-S-phase and changes in long-range replication timing domain structures. Analyses of replication timing show replication of sequences normally replicating early is delayed, whereas that normally replicating late is advanced, suggesting that replication timing regulation is abrogated in the absence of Rif1. Rif1 tightly binds to nuclear-insoluble structures at late-M-to-early-G1 and regulates chromatin-loop sizes. Furthermore, Rif1 colocalizes specifically with the mid-S replication foci. Thus, Rif1 establishes the mid-S replication domains that are restrained from being activated at early-S-phase. Our results indicate that Rif1 plays crucial roles in determining the replication timing domain structures in human cells through regulating higher-order chromatin architecture.

| S-EPMC3442267 | biostudies-literature

Genome-wide analysis of replication timing in preimplantation mouse embryos

Project description:Genome-wide analysis of replication timing in preimplantation mouse embryos

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Single embryo RNA-seq analysis in RIF1 depleted preimplantation mouse embryos

Project description:RNAseq datasets from control and RIF1-depleted mouse embryos to address whether RIF1 depletion results in changes in gene expression. siRNA was microinjected at the zygote stage and controls (embryos injected with siRNA control) and RIF1-depleted embryos (embryos injected with siRNA against Rif1) were collected either at the 4-cell or at the 8-cell stage. RNAseq was performed using SMART-Seq2 in single embryos.

2025-03-18 | GSE262789 | GEO

Rif1 regulates initiation timing of late replication origins throughout the S. cerevisiae genome.

Project description:Chromosomal DNA replication involves the coordinated activity of hundreds to thousands of replication origins. Individual replication origins are subject to epigenetic regulation of their activity during S-phase, resulting in differential efficiencies and timings of replication initiation during S-phase. This regulation is thought to involve chromatin structure and organization into timing domains with differential ability to recruit limiting replication factors. Rif1 has recently been identified as a genome-wide regulator of replication timing in fission yeast and in mammalian cells. However, previous studies in budding yeast have suggested that Rif1's role in controlling replication timing may be limited to subtelomeric domains and derives from its established role in telomere length regulation. We have analyzed replication timing by analyzing BrdU incorporation genome-wide, and report that Rif1 regulates the timing of late/dormant replication origins throughout the S. cerevisiae genome. Analysis of pfa4Δ cells, which are defective in palmitoylation and membrane association of Rif1, suggests that replication timing regulation by Rif1 is independent of its role in localizing telomeres to the nuclear periphery. Intra-S checkpoint signaling is intact in rif1Δ cells, and checkpoint-defective mec1Δ cells do not comparably deregulate replication timing, together indicating that Rif1 regulates replication timing through a mechanism independent of this checkpoint. Our results indicate that the Rif1 mechanism regulates origin timing irrespective of proximity to a chromosome end, and suggest instead that telomere sequences merely provide abundant binding sites for proteins that recruit Rif1. Still, the abundance of Rif1 binding in telomeric domains may facilitate Rif1-mediated repression of non-telomeric origins that are more distal from centromeres.

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