LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [Repli-seq]
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ABSTRACT:
PROVIDER: PRJNA661444 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12588570_1.fastq.gz | Fastqsanger.gz | |||
| SRR12588570_2.fastq.gz | Fastqsanger.gz | |||
| SRR12588571_1.fastq.gz | Fastqsanger.gz | |||
| SRR12588571_2.fastq.gz | Fastqsanger.gz | |||
| SRR12588572_1.fastq.gz | Fastqsanger.gz |
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Project description:The chromatin-based rules governing the selection and activation of replication origins remain to be elucidated. It is believed that DNA replication initiates from open chromatin domains, thus replication origins residing in regulatory elements that are located at open and active chromatin. However, we report here that lysine specific demethylase 1 (LSD1), which biochemically catalyzes H3K4me1/2 demethylation to favor chromatin condensation, interacts with the DNA replication machinery. We found that LSD1 level peaks in early S phase. We demonstrated that LSD1 promotes DNA replication by facilitating origin firing in euchromatic regions and through regulating replication timing. Indeed, euchromatic zones enriched in H3K4me2 are the preferred sites for pre-RC binding in early replication. Remarkably, LSD1 deficiency leads to a genome-wide switch from early to late in replication timing. We showed that LSD1-promoted DNA replication is mechanistically linked to the loading of TICRR (TopBP1-Interacting Checkpoint and Replication Regulator) onto the pre-RC and subsequent recruitment of the initiator Cdc45 during origin firing. Together, these results reveal an unexpected role for LSD1 in euchromatic origin firing and replication timing.
2022-03-07 | GSE157470 | GEO
Project description:The chromatin-based rules governing the selection and activation of replication origins remain to be elucidated. It is believed that DNA replication initiates from open chromatin domains, thus replication origins residing in regulatory elements that are located at open and active chromatin. However, we report here that lysine specific demethylase 1 (LSD1), which biochemically catalyzes H3K4me1/2 demethylation to favor chromatin condensation, interacts with the DNA replication machinery. We found that LSD1 level peaks in early S phase. We demonstrated that LSD1 promotes DNA replication by facilitating origin firing in euchromatic regions and through regulating replication timing. Indeed, euchromatic zones enriched in H3K4me2 are the preferred sites for pre-RC binding in early replication. Remarkably, LSD1 deficiency leads to a genome-wide switch from early to late in replication timing. We showed that LSD1-promoted DNA replication is mechanistically linked to the loading of TICRR (TopBP1-Interacting Checkpoint and Replication Regulator) onto the pre-RC and subsequent recruitment of the initiator Cdc45 during origin firing. Together, these results reveal an unexpected role for LSD1 in euchromatic origin firing and replication timing.
2022-03-07 | GSE157469 | GEO
Project description:The chromatin-based rules governing the selection and activation of replication origins remain to be elucidated. It is believed that DNA replication initiates from open chromatin domains, thus replication origins residing in regulatory elements that are located at open and active chromatin. However, we report here that lysine specific demethylase 1 (LSD1), which biochemically catalyzes H3K4me1/2 demethylation to favor chromatin condensation, interacts with the DNA replication machinery. We found that LSD1 level peaks in early S phase. We demonstrated that LSD1 promotes DNA replication by facilitating origin firing in euchromatic regions and through regulating replication timing. Indeed, euchromatic zones enriched in H3K4me2 are the preferred sites for pre-RC binding in early replication. Remarkably, LSD1 deficiency leads to a genome-wide switch from early to late in replication timing. We showed that LSD1-promoted DNA replication is mechanistically linked to the loading of TICRR (TopBP1-Interacting Checkpoint and Replication Regulator) onto the pre-RC and subsequent recruitment of the initiator Cdc45 during origin firing. Together, these results reveal an unexpected role for LSD1 in euchromatic origin firing and replication timing.
2022-03-07 | GSE157468 | GEO
Project description:LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing
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Project description:LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [ChIP-seq]
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Project description:This SuperSeries is composed of the SubSeries listed below.
2022-03-07 | GSE157471 | GEO
Project description:genome-wide analysis of replication timing by repli-chip and repli-seq
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Project description:Mouse ESC 46C replication timing has been assessed by repli-chip.
2017-07-28 | GSE95090 | GEO
Project description:How early- and late-firing origins are selected on eukaryotic chromosomes is largely unknown. Here we show that Mrc1, a conserved factor required for stabilization of stalled replication forks, selectively binds to the early-firing origins in a manner independent of Cdc45 and Hsk1 kinase in fission yeast. In mrc1∆ (and in swi1∆ to some extent), efficiency of firing is stimulated and its timing is advanced selectively at those origins that are normally bound by Mrc1. In contrast, the late or inefficient origins which are not bound by Mrc1 are not activated in mrc1∆. The enhanced firing and precocious Cdc45 loading at Mrc1-bound early-firing origins are not observed in a checkpoint mutant of mrc1, suggesting that non-checkpoint function is involved in maintaining the normal program of early-firing origins. We propose that pre-firing binding of Mrc1 is an important marker of early-firing origins which are precociously activated by the absence this protein. Mrc1 binding profiles at G1/S boundary or early S-phase in wild type vs hsk1-89 mutant.
2011-03-26 | GSE28182 | GEO
Project description:This track is produced as part of the ENCODE Project. This track shows genome-wide assessment of DNA replication timing in cell lines using the sequencing-based "Repli-seq" methodology (see below). Replication timing is known to be an important feature for epigenetic control of gene expression that usually operates at a higher-order level than at the level of specific genes. For each experiment (cell line, replicate), replication timing was ascertained by the isolation and sequencing of newly replicated DNA from six cell cycle fractions: G1/G1b, S1, S2, S3, S4, G2 (six fraction profile). Replication patterns are visualized as a continuous function based on sequencing tag density (Percentage-normalized Signal) and as a wavelet-smoothed transform of the six fraction profile (Wavelet-smoothed Signal). Replication peaks corresponding to replication initiation zones (Peaks) and valleys corresponding to replication termination zones (Valleys) were determined from local maxima and minima, respectively, in the wavelet-smoothed signal data. A measure of relative copy number at each genomic location (Summed Densities) was determined by summing the normalized tag density values of each cell cycle fraction at that location (equals one replicated genome equivalent). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Cells were grown according to the approved ENCODE cell culture protocols. Repli-seq was performed as described by Hansen et al. (2010). Briefly, newly replicated DNA was labeled in vivo with a pulse of 5-bromo-2-deoxyuridine (BrdU), cells were fractionated into six different parts of the cell cycle by flow cytometry according to DNA content, cell cycle fractionated DNA was sonicated and an anti-BrdU monoclonal antibody was used to isolate the newly replicating DNA. Fragment ends were sequenced using the Illumina Genome Analyzer II or HiSeq platforms (36 bp reads). Some experiments (BJ, K562, BG02ES, GM06990) were originally performed and mapped to an earlier version of the human reference genome NCBI36/hg18 (Hansen et al., 2010) and were remapped to the more recent reference genome GRCh37/hg19. Uniquely mapping high-quality reads were mapped to the genome minus the Y chromosome. Replication signals within each six cell cycle fraction were derived from the density of sequence tags mapping within a 50 kb sliding window (stepped 1 kb across the genome); these densities were normalized to 4 million tags per genome. To avoid variation due to copy number or sequence bias, cell cycle-specific replication signals at each location were determined as a percentage of the sum of the six normalized tag density signals (Percentage-normalized Signal). To transform the six fraction replication signals into one track (Wavelet-smoothed Signal), the percentage-normalized signals at each location were used to calculate a weighted average value based on the average DNA content of each fraction according to flow cytometry [higher values correspond to earlier replication; formula=(0.917*G1b)+(0.750*S1)+(0.583*S2)+(0.417*S3)+(0.250*S4)+(0*G2)]. These weighted average data were smoothed by wavelet transformation [J7 level, corresponding to a scale of 128 kb; see Thurman et al. (2007)]. Replication initiation zones were flagged by determining local maxima in the wavelet-smoothed data (Peaks) and, similarly, replication termination zones were flagged by local minima (Valleys). The sum of the 4 million normalized replication tag densities correspond to replication of one genome and can, therefore, be used as a measure of relative genomic copy number (Summed Densities). This is useful for evaluation of unusual replication patterns, such as "biphasic" ones where replication has both early and late components [as described by Hansen et al. (2010)].
2012-04-26 | E-GEOD-34399 | biostudies-arrayexpress