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LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [ChIP-seq]

ABSTRACT: LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [ChIP-seq]

PROVIDER: PRJNA661442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12588566.fastq.gz	Fastqsanger.gz
	SRR12588567.fastq.gz	Fastqsanger.gz
	SRR12588568.fastq.gz	Fastqsanger.gz
	SRR12588569.fastq.gz	Fastqsanger.gz
	SRR12626359_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [ChIP-seq]

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

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [RNA-seq]

2022-03-07 | GSE157468 | GEO

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [Repli-seq]

2022-03-07 | GSE157470 | GEO

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing

Project description:LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing

| PRJNA661437 | ENA

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [RNA-seq]

Project description:LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [RNA-seq]

| PRJNA661443 | ENA

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [Repli-seq]

Project description:LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing [Repli-seq]

| PRJNA661444 | ENA

LSD1 is required for euchromatic origin firing and replication timing.

Project description:The chromatin-based rule governing the selection and activation of replication origins remains to be elucidated. It is believed that DNA replication initiates from open chromatin domains; thus, replication origins reside in open and active chromatin. However, we report here that lysine-specific demethylase 1 (LSD1), which biochemically catalyzes H3K4me1/2 demethylation favoring chromatin condensation, interacts with the DNA replication machinery in human cells. We find that LSD1 level peaks in early S phase, when it is required for DNA replication by facilitating origin firing in euchromatic regions. Indeed, euchromatic zones enriched in H3K4me2 are the preferred sites for the pre-replicative complex (pre-RC) binding. Remarkably, LSD1 deficiency leads to a genome-wide switch of replication from early to late. We show that LSD1-engaged DNA replication is mechanistically linked to the loading of TopBP1-Interacting Checkpoint and Replication Regulator (TICRR) onto the pre-RC and subsequent recruitment of CDC45 during origin firing. Together, these results reveal an unexpected role for LSD1 in euchromatic origin firing and replication timing, highlighting the importance of epigenetic regulation in the activation of replication origins. As selective inhibitors of LSD1 are being exploited as potential cancer therapeutics, our study supports the importance of leveraging an appropriate level of LSD1 to curb the side effects of anti-LSD1 therapy.

| S-EPMC9005705 | biostudies-literature

LSD1 Facilitates Euchromatic Origin Firing and Regulates Replication Timing

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

2022-03-07 | GSE157471 | GEO

KMT2C/KMT2D-dependent H3K4me1 mediates DNA replication timing and origin firing

Project description:KMT2C/KMT2D-dependent H3K4me1 mediates DNA replication timing and origin firing

| PRJNA1164200 | ENA

Rif1 is a global regulator of timing of replication origin firing in fission yeast

Project description:One of the long-standing questions in eukaryotic DNA replication is the mechanisms that determine where and when a particular segment of the genome is replicated. Cdc7/Hsk1 is a conserved kinase required for initiation of DNA replication, and may affect the site selection and timing of origin firing. We identified rif1∆, a null mutant of rif1+, a conserved telomere binding factor, as an efficient bypass mutant of fission yeast hsk1. Extensive deregulation of dormant origins over a wide range of the chromosomes occurs in rif1∆ in the presence or absence of HU. At the same time, many early-firing, efficient origins are suppressed or delayed in firing timing in rif1∆. Rif1 binds not only to telomeres but also to many specific locations on the arm segments that only partially overlap with the pre-Replicative Complex assembly sites, although Rif1 tends to bind in the vicinity of the late/ dormant origins activated in rif1∆. The binding to the arm segments occurs through M to G1 phase in a manner independent of Taz1 and appears to be essential for the replication timing program during normal cell cycle. Our data demonstrate that Rif1 is a critical determinant of origin activation program on the fission yeast chromosomes. BrdU incorporation profiles at early S-phase in Wild vs rif1∆. Cdc45 binding profiles at early S-phase in Wild vs rif1∆. Rif1 binidng sites aroud G1/S boudary and at M-phase. Mcm4 binding sites in wild, hsk1-89 temperature mutant and rif1∆.

2011-12-13 | GSE34369 | GEO

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