Loss of H3K9 tri-methylation alters mitotic chromosome compaction and transcription factor retention during mitosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA802124 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17832738_1.fastq.gz | Fastqsanger.gz | |||
| SRR17832738_2.fastq.gz | Fastqsanger.gz | |||
| SRR17832739_1.fastq.gz | Fastqsanger.gz | |||
| SRR17832739_2.fastq.gz | Fastqsanger.gz | |||
| SRR17832740_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases and Polycomb Repressor Complexes, bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Here we show that enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a and Glp, are also retained on mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants were rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1/Suv39h2 double-null mouse ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.
2023-01-25 | PXD039521 | Pride
Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases (DNMTs) and Polycomb Repressor Complexes (PRCs), bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a, GLP are also retained by mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes that are associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants was rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1,2 double null ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.
2022-10-12 | PXD030771 | Pride
Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases (DNMTs) and Polycomb Repressor Complexes (PRCs), bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a, GLP are also retained by mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes that are associated with increased H3S10ph and H3K27me3 levels. Despite these differences, chromatin accessibility, as measured by ATAC-seq, was broadly similar between genotypes. Chromosome size and centromere compaction in these mutants was rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1,2 double null ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.
2023-01-17 | GSE195767 | GEO
Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases and polycomb repressor complexes, binds to chromosomes throughout mitosis and their depletion results in increased chromosome size. In the present study, we show that enzymes that catalyze H3K9 methylation, such as Suv39h1, Suv39h2, G9a and Glp, are also retained on mitotic chromosomes. Surprisingly, however, mutants lacking histone 3 lysine 9 trimethylation (H3K9me3) have unusually small and compact mitotic chromosomes associated with increased histone H3 phospho Ser10 (H3S10ph) and H3K27me3 levels. Chromosome size and centromere compaction in these mutants were rescued by providing exogenous first protein lysine methyltransferase Suv39h1 or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wild-type versus Suv39h1/Suv39h2 double-null mouse embryonic stem cells revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.
| S-EPMC10113154 | biostudies-literature
Project description:In mammals, chromosome-wide regulatory mechanisms ensure a balance of X-linked gene dosage between males (XY) and females (XX). In female cells, expression of genes from one of the two X-chromosomes is curtailed, with selective accumulation of Xist-RNA, Xist-associated proteins, specific histone modifications (eg. H3K27me3) and Barr body formation observed throughout interphase. Using chromosome flow-sorting, we show that during mitosis, Xist-associated proteins dissociate from inactive X (Xi) chromosomes, while high levels of H3K27me3 and increased compaction of the Xi relative to active X (Xa), are retained. Proteomic comparison of mitotic Xi and Xa revealed, unexpectedly, that components of Hbo1 and Msl/Mof histone acetyltransferase complexes co-enrich with Xa, while inhibitors of histone acetylation co-enrich with Xi. Furthermore, inhibition of Hbo1 or deletion of Msl/Mof components functionally abolishes mitotic differences in H3K27me3 marking and chromosome compaction. These data uncover critical roles for acetylation pathways in preserving X chromosome properties during mitosis.
2025-05-23 | PXD054014 | Pride
Project description:Cold-induced chromatin compaction and nuclear retention of clock mRNAs resets the circadian rhythm
| PRJNA564264 | ENA
Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
2024-02-03 | GSE224640 | GEO
Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
2024-02-03 | GSE224639 | GEO
Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
2024-02-03 | GSE224638 | GEO
Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
2024-02-03 | GSE224636 | GEO