G1 length dictates heterochromatin landscape [CUT&Tag]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1101491 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28722884_1.fastq.gz | Fastqsanger.gz | |||
| SRR28722884_2.fastq.gz | Fastqsanger.gz | |||
| SRR28722885_1.fastq.gz | Fastqsanger.gz | |||
| SRR28722885_2.fastq.gz | Fastqsanger.gz | |||
| SRR28722886_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 22 |
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Project description:Stem cells have lower facultative heterochromatin as defined by trimethylation of histone H3 lysine 27 (H3K27me3) compared to differentiated cells. However, the mechanisms underlying these differential H3K27me3 levels remain elusive. Because H3K27me3 levels are diluted two-fold in every round of replication and then restored through the rest of the cell cycle, we reasoned that the cell cycle length could be a key regulator of total H3K27me3 levels. Here, we demonstrate that a fast cell cycle sets low levels of H3K27me3 in serum-grown murine embryonic stem cells (mESCs). Extending the G1 phase leads to an increase in global H3K27me3 in mESCs due to the formation of de novo Polycomb domains, and the length of the G1/S block correlates with the extent of gain in H3K27me3, arguing that levels of the modification depend on the time available between successive rounds of replication. Similarly, accelerating the G1 phase in HEK293 cells decreases H3K27me3 levels. Finally, we applied this principle in tumor cells harboring a dominant negative H3K27M allele that reduces H3K27me3 levels. In these cells, extending G1 increases H3K27me3 levels, pointing to an unexpected means to rescue the effect of oncohistones. Our results suggest cell cycle length as a universal mechanism to modulate heterochromatin formation and, thus, cellular identity.
2025-03-10 | GSE264215 | GEO
Project description:Stem cells have lower facultative heterochromatin as defined by trimethylation of histone H3 lysine 27 (H3K27me3) compared to differentiated cells. However, the mechanisms underlying these differential H3K27me3 levels remain elusive. Because H3K27me3 levels are diluted two-fold in every round of replication and then restored through the rest of the cell cycle, we reasoned that the cell cycle length could be a key regulator of total H3K27me3 levels. Here, we demonstrate that a fast cell cycle sets low levels of H3K27me3 in serum-grown murine embryonic stem cells (mESCs). Extending the G1 phase leads to an increase in global H3K27me3 in mESCs due to the formation of de novo Polycomb domains, and the length of the G1/S block correlates with the extent of gain in H3K27me3, arguing that levels of the modification depend on the time available between successive rounds of replication. Similarly, accelerating the G1 phase in HEK293 cells decreases H3K27me3 levels. Finally, we applied this principle in tumor cells harboring a dominant negative H3K27M allele that reduces H3K27me3 levels. In these cells, extending G1 increases H3K27me3 levels, pointing to an unexpected means to rescue the effect of oncohistones. Our results suggest cell cycle length as a universal mechanism to modulate heterochromatin formation and, thus, cellular identity.
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Project description:Stem cells have lower facultative heterochromatin as defined by trimethylation of histone H3 lysine 27 (H3K27me3) compared to differentiated cells. However, the mechanisms underlying these differential H3K27me3 levels remain elusive. Because H3K27me3 levels are diluted two-fold in every round of replication and then restored through the rest of the cell cycle, we reasoned that the cell cycle length could be a key regulator of total H3K27me3 levels. Here, we demonstrate that a fast cell cycle sets low levels of H3K27me3 in serum-grown murine embryonic stem cells (mESCs). Extending the G1 phase leads to an increase in global H3K27me3 in mESCs due to the formation of de novo Polycomb domains, and the length of the G1/S block correlates with the extent of gain in H3K27me3, arguing that levels of the modification depend on the time available between successive rounds of replication. Similarly, accelerating the G1 phase in HEK293 cells decreases H3K27me3 levels. Finally, we applied this principle in tumor cells harboring a dominant negative H3K27M allele that reduces H3K27me3 levels. In these cells, extending G1 increases H3K27me3 levels, pointing to an unexpected means to rescue the effect of oncohistones. Our results suggest cell cycle length as a universal mechanism to modulate heterochromatin formation and, thus, cellular identity.
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Project description:Overall, this paper demonstrated that the speed of the cell cycle determines the level of H3K27me3 in serum-grown murine embryonic stem cells, with extended G1 phase leading to increased global H3K27me3 levels and accelerated cell cycle leading to decreased H3K27me3 levels. This MassIVE entry contains mass spectrometry files that measured H3K27me3 levels using propionic anhydride derivatization methods.
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Project description:DNA replication requires the recruitment of a pre-replication complex facilitated by Origin Recognition Complex (ORC) onto the chromatin during G1 phase of the cell cycle. The ORC-associated protein (ORCA/LRWD1) stabilizes ORC on chromatin. Here, we evaluated the genome-wide distribution of ORCA using ChIP-seq during specific time points of G1. ORCA binding sites on the G1 chromatin are dynamic and temporally regulated. ORCA association to specific genomic sites decreases as the cells progressed towards S-phase. The majority of the ORCA-bound sites represent replication origins that also associate with the repressive chromatin marks H3K9me3 and methylated-CpGs, consistent with ORCA-bound origins initiating DNA replication late in S-phase. Further, ORCA directly associates with the repressive marks and interacts with the enzymes that catalyze these marks. Regions that associate with both ORCA and H3K9me3, exhibit diminished H3K9 methylation in ORCA-depleted cells, suggesting a role for ORCA in recruiting the H3K9me3 mark at certain genomic loci. Similarly, DNA methylation is altered at ORCA-occupied sites in cells lacking ORCA. Furthermore, repressive chromatin marks influence ORCA's binding on chromatin. We propose that ORCA coordinates with the histone and DNA methylation machinery to establish a repressive chromatin environment at a subset of origins, which primes them for late replication.
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